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DENTAL SCIENCE, MATERIALS AND TECHNOLOGY
PERIODONTAL DISEASE: SYMPTOMS, TREATMENT AND PREVENTION No part of this digital document may be reproduced, stored in a retrieval system or transmitted in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services.
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DENTAL SCIENCE, MATERIALS AND TECHNOLOGY
PERIODONTAL DISEASE: SYMPTOMS, TREATMENT AND PREVENTION
SHO L. YAMAMOTO EDITOR
Nova Biomedical Books New York
Copyright © 2011 by Nova Science Publishers, Inc. All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical photocopying, recording or otherwise without the written permission of the Publisher. For permission to use material from this book please contact us: Telephone 631-231-7269; Fax 631-231-8175 Web Site: http://www.novapublishers.com NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book. The Publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers‘ use of, or reliance upon, this material. Any parts of this book based on government reports are so indicated and copyright is claimed for those parts to the extent applicable to compilations of such works. Independent verification should be sought for any data, advice or recommendations contained in this book. In addition, no responsibility is assumed by the publisher for any injury and/or damage to persons or property arising from any methods, products, instructions, ideas or otherwise contained in this publication. This publication is designed to provide accurate and authoritative information with regard to the subject matter covered herein. It is sold with the clear understanding that the Publisher is not engaged in rendering legal or any other professional services. If legal or any other expert assistance is required, the services of a competent person should be sought. FROM A DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS. Additional color graphics may be available in the e-book version of this book. Library of Congress Cataloging-in-Publication Data Periodontal disease : symptoms, treatment, and prevention / editor, Sho L. Yamamoto. p. ; cm. Includes bibliographical references and index. ISBN 978-1-61122-112-1 (eBook) 1. Periodontal disease. I. Yamamoto, Sho L. [DNLM: 1. Periodontal Diseases. WU 240] RK361.P453 2010 617.6'32--dc22 2010033087
New York
Contents Preface
vii
Chapter I
Aesthetic Periodontal Therapy – Root Coverage A. L. Dumitrescu, Liviu Zetu and Silvia Teslaru
Chapter II
Periodontal Diseases in Children and Adolescents: Clinical Features and Molecular Biological Analyses Kazuhiko Nakano, Atsuo Amano and Takashi Ooshima
Chapter III
Biomechanics of Rehabilitating the Perioprosthetic Patient Petros Koidis and Manda Marianthi
Chapter IV
Biomarkers of Periodontal Disease: Past, Present and Future Challenges Fionnuala T. Lundy
Chapter V
Inflammatory Mediators and Oxidative Stress in Periodontal Disease Luigi F. Rodella, Paolo Brunamonti Binello, Barbara Buffoli, Davide Merigo and Mauro Labanca
Chapter VI
Tobacco: A Risk Factor for Periodontal Disease Nouf Al-Shibani, Nawaf Labban, Eman Allam, and L. Jack Windsor
Chapter VII
A Novel Cytodiagnostic Fluorescence Assay for the Diagnosis of Periodontitis Marco Giannelli, Lucia Formigli and Daniele Bani
Chapter VIII
The Healthy Periodontium, the Diseased Periodontium Leena Palomo and Nabil Bissada
Chapter IX
Clinical Effects of 2% Chlorhexidine Gel on Patients Undergoing Orthodontic Treatment Abdolreza Jamilian, Mahmood Ghasemi Dariush Gholami and Bita Kaveh
1
31 67
93
107
121
137 153
205
vi Chapter X
Contents Periodontal Disease and Systemic Diseases: Interrelationships and Interactions Giuseppe Pizzo, Rosario Guiglia and Giuseppina Campisi
Chapter XI
Obesity Revised Ayse Basak Cinar
Chapter XII
Invasion of Host Cells by Porphyromonas Gingivalisin Polymicrobial Infection Atsushi Saito, Satoru Inagaki, Eitoyo Kokubu, Ryuta Kimizuka and Kazuyuki Ishihara
Chapter XIII
HMGB1: A Novel Inflammatory Mediator in Chronic Periodontitis Yoko Morimoto-Yamashita, Masayuki Tokuda, Kiyoshi Kikuchi, Ikuro Maruyama, Mitsuo Torii, and Ko-ichi Kawahara
215 247
257
273
Chapter XIV
Risk Factors for Chronic Periodontal Diseases Daniela da Silva Feitosa, Mauro Pedrine Santamaria, Márcio Zaffalon Casati, Enilson Antonio Sallum, Francisco Humberto Nociti Júnior and Sérgio de Toledo
287
Chapter XV
The Role of Antimicrobial Peptides in Periodontal Disease Suttichai Krisanaprakornkit and Sakornrat Khongkhunthian
321
Index
353
Preface Periodontal disease is a chronic bacterial infection characterized by persistent inflammation, connective tissue breakdown and alveolar bone destruction. The chronic inflammation associated with periodontal disease represents the host response to bacterial plaque, mediated by the environment in which the response occurs. This book presents topical research data in the study of periodontal disease, including aesthetic periodontal therapy and root coverage techniques; clinical features of periodontal diseases in children and adolescents; biomechanics and the perioprosthetic patient; maternal periodontitis and perinatal outcomes; identifying patients with enhanced disease susceptibility in periodontal disease; and inflammatory mediators and oxidative stress in periodontal disease. Chapter I - Aesthetic considerations have influenced the management of dental maladies in varying degrees for many years. For many years the goals of periodontal surgery have been determined by functional aspects only. During recent years periodontal surgery has shifted its focus from achieving more functional goals toward a combination of both good functional and esthetic results. While accomplishing the best possible functional result, esthetics should not only be maintained, but also enhanced. Sometimes the esthetic outcome is the only important factor and function becomes secondary (e.g. treatment of recessions or the creation of papillae). Predictability becomes the key word in this type of periodontal surgery. Patient awareness and expectations have increased recently to the point that less than optimal esthetics is no longer an acceptable outcome. Periodontal plastic surgery would accordingly be defined as ―surgical procedures performed to prevent or correct anatomic, developmental, traumatic or disease induced defects in the gingiva, alveolar mucosa or bone‖. The present chapter is presenting and discussing the clinical outcomes of several root coverage techniques: pedicle soft tissue grafts, rotational flaps, coronally advanced flap, semilunar flap, free soft tissue graft, nonsubmerged grafts, submerged grafts etc. Chapter II - The clinical features of periodontal diseases in children and adolescents differ from those in adults. Periodontitis is extremely rare in children, except those complicated with certain kinds of systemic diseases, whereas gingivitis is commonly encountered. Childhood gingivitis can be reversed by professional mechanical tooth cleaning in combination with tooth brushing instruction. On the other hand, gingivitis becomes increasingly prevalent with age through the adolescent period, and early diagnosis and appropriate interventions are necessary to prevent the onset of marginal periodontitis during adolescence. Since most children with periodontitis possess a background of abnormal immune responses, they have a lower likelihood of good prognosis,even though diligent interventions are performed. Other types of periodontal diseases include gingival recession,
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which is mainly caused by traumatic occlusion, and gingival overgrowth, which has a hereditary background and is associated with specific medication such as antiepilepticphenytoin. In addition, cases with a rapid loss of gingival attachment and alveolar bone due to mechanical injury at the periodontal sulcus, termed ―acute periodontitis,‖ are also encountered. Furthermore, an unintentional attachment loss, when materials such as small plastic tubes being fitted to the teeth are inserted, is a unique type of periodontitis in young children. It should be noted that periodontitis associated with anatomical anomalies, which are derived from fragile periodontal attachment, is also encountered. Considering the etiology of periodontitis, it is important to identify periodontitis-related bacterial species, since the disease is generally known to be caused by specific bacteria. However, most of those belong to the obligate anaerobic group, and it is difficult and timeconsuming to isolate them. On the other hand, recent developments in molecular biological techniques have enabled rapid identification of species using bacterial DNA extracted from various kinds of clinical specimens. Such approaches do not require isolation of viable bacteria and even small amounts of DNA can be detected using PCR techniques. With such modern techniques, the author have evaluated the distribution of periodontal bacterial species in children, changes of species in the same subjects over a long interval, combinations of species simultaneously detected, and mother-to-child transmission. In addition, the distributions of bacterial species in children with Down‘s syndrome and other developmental disabilities have been analyzed. The authors‘ results have provided valuable information regarding bacterial profiles in clinical specimens, which should lead to further beneficial methods for clinical use in the near future. Chapter III - In advanced perioprosthetic cases where the periodontium‘s integrity is severely compromised and the dental barrier‘s function is extremely disrupted, the biomechanical response to the extrinsic mechanical stimuli of the system including the prosthetic restoration supported by the biological tissues is quite altered. The differentiated altered experience of the functional loading due to the lowered periodontium‘s threshold along with the apical shift of the system fulcrum due to the periodontium‘s structure reduction require a modified design of the restoration‘s metal framework as a critical factor in the system‘s survival in order to secure the expected longevity of both the restorative and biological structures, capturing the failure initiation of either progressive tissular or technical collapse. So, the purpose of the present study was to: a. analyze the way by which the periodontium reacts to the developing forces and how its integrity is related to the experience of the stress field on the perioprosthetic patient; b. determine the parameters defining the tooth prognosis in the perioprosthetic patient and how the restoration type is involved; c. report the clinical significance of tooth splinting by cantilever cross arch fixed partial denture applied on the perioprosthetic patient and the way it is related to the response of the reduced periodontium and finally d. investigate the clinical significance of the specific design of the metal framework in cantilever cross-arch fixed partial dentures via a theoretical finite element model. Chapter IV - Periodontal disease is a chronic bacterial infection characterised by persistent inflammation, connective tissue breakdown and alveolar bone destruction. The chronic inflammation associated with periodontal disease represents the host response to bacterial plaque, mediated by the environment in which the response occurs. Periodontitis is both site-specific and episodic in nature and thus biomarker development could prove
Preface
ix
invaluable in identifying sites with active disease, predicting sites that may develop disease, monitoring response to therapy or identifying patients with enhanced disease susceptibility. In periodontal disease gingival crevicular fluid (GCF) flows from the gingival microcirculation into the periodontal pockets and the volume increases in proportion to the severity of the local inflammatory process. The study of GCF samples, from defined sites of chronic periodontal inflammation, allows non-invasive access to an inflammatory exudate that could be used for biomarker discovery. GCF contains proteins synthesised and secreted in the inflamed gingival tissues and carried by the GCF to the gingival crevice/pocket. Here, they are augmented by proteins released from bacteria and host cells, particularly polymorphonuclear leukocytes (PMNs), present in the periodontal pocket. The constituents of GCF are therefore derived from a number of sources including microbial plaque, host inflammatory cells, serum and tissue breakdown products. Saliva has also been studied in the search for biomarkers of periodontal disease. Saliva is a more complex fluid, comprising glandular secretions, components of GCF, components of serum and also particles (including bacteria) from a variety of oral and airway sources. Although saliva has the advantage of being easily collected, its biochemical complexity may hinder detection of biomarkers specific for periodontal disease. Furthermore the fact that saliva bathes the whole mouth negates the use of salivary biomarkers for site-specific identification or monitoring of periodontal disease. Despite an impressive list of possibilities, biomarkers have yet to reach routine clinical use as reasonable predictors of periodontal status. This chapter reviews the analysis of GCF and saliva for monitoring periodontal health and disease. Potentially important biomarkers of disease in both GCF and saliva are highlighted and their merits are described in further detail. Putative biomarkers from both host and bacterial sources are considered and the use of multiple biomarkers is discussed. Following the technological revolution in both genomic and proteomic analysis over the last decade it is tempting to speculate that the next decade could bring much waited progress in the field of biomarker identification and application in the field of periodontal disease. Chapter V - Periodontal disease represents today the main cause of teeth loss after the third decade of life. About 60% of dental extractions are due to etiopathogenetic periodontal factors. After 35 years, the frequency of marginal periodontal disease varies from 80% to 100% of world population, depending on statistical method used and the demographic areas considered, showing a similar frequency in both sexes, slightly higher in female. Two important and interrelated factors are involved in its physiopathological progression: 1) the activation of immune system and the release of inflammatory mediators, such as IL-1β, IL-6 and TNF-α, which could overflow into the blood system and induce a systemic inflammatory response; 2) the production of oxygen radicals and their related metabolites. A recent focus of the dental research is the individuation of biomarkers, which can be easily used as diagnostic tools. Among them, metalloproteinases (MMPs) and heat shock proteins (HSPs) could provide potential biomarkers, which could be useful for evaluating both the periodontitis development and the incidence of the related cardiovascular diseases. Recent studies, in fact, have shown a direct correlation between periodontal and cardiovascular diseases: in particular, both diseases have systemic and local causes, and the constant bacterial contamination of oral cavity could be linked not only to periodontopathy but also to the development of cardiovascular diseases.
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To date, the periodontal disease therapy available is based on the individuation and the elimination of the causing factors. Nevertheless, new innovative surgical and pharmacological therapies could be developed. The aim of this work is to review the literature data focusing on the role of inflammatory mediators and oxidative stress in periodontal disease and related factors. Chapter VI - Periodontal disease results from complex interactions between infectious agents and host factors. The disease expression can be modified by environmental, acquired, and genetic risk factors. Tobacco usage, especially smoking, is considered a major modifiable risk factor for periodontal disease. In addition to periodontal disease, tobacco usage is also a risk factor for oral cancer and its recurrence, dental cariesand congenital defects in children from mothers who smoke while pregnant. In periodontal disease, smokers have deeper probing depths, more gingival recession, more alveolar loss and more furcation involvement than non-smokers. They also show less favorable responses to various kinds of periodontal treatments including non-surgical, surgical, regenerative procedures and dental implants. It is clear from epidemiology studies that tobacco usage is correlated with periodontal disease. This chapter reviews the evidence for the association between periodontal disease and tobacco, and describes what is currently known about how tobacco and its components affect the periodontal tissues that result in tissue damage. Chapter VII - A topical issue in periodontology is to find objective diagnostic methods which may be combined with the classical clinical inspection parameters to yield a reliable grading of the severity and extent of periodontal disease. This study deals with a novel cytodiagnostic fluorescence test, performed on exfoliation samples taken from periodontal/oral tissues, useful to assess the severity of periodontal disease. Twenty-one patients with different degrees of periodontitis were subjected to clinical and histopathological grading and the results compared with those obtained from the cytodiagnostic fluorescence assay. The author found that the amount of blood cells (polymorphonuclear and mononuclear leukocytes, erythrocytes), the occurrence of morphologically abnormal epithelial cells, and the number of spirochetes showed a statistically significant correlation with the clinical and histopathological diagnostic parameters, the latter being considered as the most reliable predictors of the severity of periodontal disease. On these grounds, the author suggest that this cytodiagnostic method may greatly help dental practitioners to achieve a chair-side, reliable and objective evaluation of the degree and activity of periodontitis at first dental visit, and to perform a targeted treatment and an accurate follow up of the patients during supportive periodontal therapy. Chapter VIII -Differentiation of health from disease is central to understanding diagnosis and treatment of periodontal diseases. It is logical to begin with an in-depth examination of the structure and physiology of the healthy periodontium. Chapter IX - Objectives: The purpose of this study was to compare the short-term clinical effects of a single intrasulcular injection of 2% chlorhexidine gluconate gel (CG) and placebo gel (PG) in orthodontic patients with fixed appliances and established gingivitis aged from 12 to 20 years. Methods and Materials: 50 patients (31 females, 19 males) were divided into two groups (CG and PG) of 50 subjects. This study was single blind randomized split mouth clinical trial. As randomly assigned by coin toss, the first permanent molars on the right or left side of the mouth received either CG or PG. Probing depth (PD) was measured with a Michigan 0 probe. The gingival index (GI) of Löe and SILNESS and papilla bleeding index (PBI) of
Preface
xi
MÜHLEMANN were recorded on the first permanent molars. These indices were measured at baseline, and in treatment on second, fourth, eighth, and the twelfth weeks. T-test and chisquare test were used to analyze the data. Results: T-test showed that PD was reduced in experimental group in comparison with the control group in the 4th week and following intervals (p50% of the MM-MD distance but not exceeding 75% 5: exposure of the CEJ >75'/o of the MM-MD distance up to 100%
Allocation of these codes does not imply that the extent of recession is equally dispersed about the facial or lingual midpoints of the area of exposed roots. The second digit of the IR gives the vertical extent of recession measured in whole mm on a range 0-9. The precise criteria proposed are as follows: 0: no clinical evidence of root exposure 1: as 0, but a subjective awareness of dentinal hypersensitivity is reported and/or there is clinically detectable exposure of the CEJ not extending >1 mm vertically to the gingival margin 2-8: root exposure 2-8 mm extending vertically from the CEJ to the base of the soft tissue defect 9: root exposure>8 mm from the CEJ to the base of the soft tissue defect. An asterisk is afixed to the second digit whenever the vertical component of the soft tissue defect encroaches into the muco-gingival junction or extends beyond it into alveolar mucosa. The absence of an asterisk thus implies either absence of muco-gingival junction at the indexed site or its non-involvement in the soft tissue defect. The prefixed F (or L) denotes whether gingival recession is facial {or lingual) to the involved root.
3. Gingival Biotypes The gingival morphology of the maxillary anterior region plays an important role in determining the final esthetic outcome (Fu et al., 2010). Clinical observations have led clinicians to identify two basic human periodontal forms (Ochsenbein and Ross, 1973; Claffey and Shanley, 1986; Seibert and Lindhe, 1989). The more prevalent, the thick flat type, occurs in over 85% of the patient population; the other, the thin scalloped type, occurs in less than 15% of cases (Sanavi et al., 1998). In the thick flat type there is this normal rise and fall of the gingival and bone, but there is not a great disparity between the direct facial and that found interproximally. The gingiva is thick or dense and is fibrotic in nature. Usually this type of periodontiurn has, quantitatively and qualitatively, adequate amounts of attached masticatory mucosa. The teeth found in the
Aesthetic Periodontal Therapy – Root Coverage
5
thick flat periodontium are usually characterized by being more bulbous and square in form. Contact areas are located more apically and usually are broad inciso gingivally and faciolingually. The interproximal papillae filling the space between the teeth terminate at the contact areas, hence, a flat periodontium. When irritated by tooth preparation, impression procedures, extraction, or other clinical techniques, this periodontium usually reacts with inflammation, followed by migration of the junctional epithelium apically, with resultant periodontal pocket formation or redundant tissue (Sanavi et al., 1998). Predicable soft and hard tissue contour after healing following surgery and minimal ridge resorption occurs after extractions (Kao et al., 2008). The thin scalloped type of periodontium, on the other hand, is distinguished by a pronounced disparity between the height on the direct facial and that found interproximally. The underlying bone is usually thin on the facial with dehiscences and fenestrations commonly found. Usually there is less attached masticatory mucosa, from both quantitative and qualitative perspectives. In the thin scalloped periodontium, the tooth form is usually more subtle and somewhat triangular. Contact areas are located more incisally and are small incisogingivally and faciolingually. The cervical convexity is less prominent. Since the contact areas are located more incisally, the interproximal papilla is also positioned more incisally, hence, the scalloped form. Excessive irritation of this type of periodontium usually leads to recession both facially and interproximally (Sanavi et al., 1998). In this gingival biotype after surgery it is difficult to predict where tissue will heal and stabilize and extensive ridge resorption in the apical and lingual direction usually occurs after extractions (Kao et al., 2008). Many methods have been proposed to measure gingival tissue thickness:
direct measurements (Greenberg et al., 1976) probe transparency (DeRouck et al., 2009; Kan et al., 2003). This evaluation was based on the transparancy of the periodontal probe through the gingival margin while probing the sulcus at the midfacial aspect of the examined tooth. If the outline of the underlying periodontal probe could be seen through the gingival, it was categorized as thin; if not, it was categorized as thick. ultrasonic devices (Müller et al., 2000) cone-beam computer tomography (CBCT) (Januário et al., 2008; Barriviera et al., 2009; Fu et al., 2010).
The identification of the gingival biotype may be important in clinical practice since differences in gingival and osseous architecture have been shown to exhibit a significant impact on the outcomes of periodontal therapy (Claffey and Shanley., 1986; Anderegg et al., 1995; Baldi et al., 1999), root coverage procedures (Huang et al., 2005; Hwang and Wang, 2006), orthodontic therapy (Wennström et al., 1990, 1996) and implants esthetics (Zigdon et al., 2008; De Rouck et al., 2009; Evans and Chen, 2008; Romeo et al., 2008). Hwang and Wang (2006) reviewed the current literature to verify the presence of any association between gingival thickness and root coverage outcomes.Fifteen investigations were included. All of these reported at least 0.7mm of flap thickness, although measurement locations varied. Treatment modalities included coronally advanced flap, connective tissue graft, and guided tissue regeneration with and without adjuncts. A significant moderate
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A. L. Dumitrescu, Liviu Zetu and Silvia Teslaru
correlation occurred between weighted flap thickness and weighted mean root coverage and weighted complete root coverage (r = 0.646 and 0.454, respectively; weighted mean of gingival thickness accounted for 41.7% of variability in weighted mean root coverage results and a lesser proportion (20.7%) in weighted complete root coverage (Hwang and Wang, 2006). The paradigm shift proposedby Kao et al. (2008) was that by taking into consideration the gingival tissue biotype during treatment planning, more appropriate strategies for periodontal management may be developed, resulting in more predictable treatment outcomes.
4. Root Coverage Procedures Surgical procedures used in the treatment of recession defects may basically be classified as (1) pedicle soft tissue graft procedures and (2) free soft tissue graft procedures (Wennström et al., 2008).
4.1. Pedicle Soft Tissue Grafts The pedicle graft procedures are, depending on the direct of transfer, grouped as (1) rotational flap procedures (e.g. laterally sliding flap, double papilla flap, oblique rotated flap) or (2) advanced flap procedures (e.g. coronally repositioned flap, semilunar coronally positioned flap). Regenerative procedures are also included within the group of pedicle graft procedures, i.e. rotational and advanced flap procedures involving the placement of a barrier membrane between the graft and the root or the application of enamel matrix proteins (Wennström et al., 2008). 4.1.1. Rotational Flaps Grupe and Warren (1956) introduced the first technique for covering a localized gingival recession. The laterally sliding flap consists of the removal of the collar of the gingiva around the area of recession and elevation of a full-thickness flap on the adjacent tooth.This flap is positioned laterally and sutured over the denuded root surface. The limitations of the procedure are the amount of the attached tissue and the thickness of the labial bone at the donor site. Leaving a thin labial plate exposed on the donor tooth risks recession at this site. An laterally positioned pedicle graft cannot be performed unless there is significant gingival lateral to the site of recession. A shallow vestibule also may jeopardize outcomes. Although the use of the laterally positioned pedicle graft provides an ideal color match, it often is inadequate for the treatment of multiple recessions (Kassab et al., 2010). The technique is as follows (Figure 1.): Recipient area.Initially, the recipient area for the laterally moved flap is prepared. A reverse bevel incision is made all along the soft tissue margin of the defect. After removal of the dissected pocket epithelium, the exposed root surface is thoroughly curetted. Two superficial incisions are then delineating a 3 mm wide recipient area, at the one side of the
Aesthetic Periodontal Therapy – Root Coverage
7
defect as well as apical to the defect, where the epithelium together with the outer portion of the connective tissue is removed by sharp dissection (Weneström et al., 2008). The flap design is outlined by two vertical incisions that extended from the horizontal incision to several millimeters apically to the mucogingival junction. A horizontal incision is performed either at the gingival or 3 mm apically, following the marginal gingival contour, thus joining the vertical incisions. A beveled linear horizontal incision is performed to optimize the content of keratized tissue in the flap when the donor site is an edentulous site. The flap is elevated as full thickness in the portion adjacent to the recession and as partial thickness in the portion distal to the recession. Partial-thickness dissection is continued apically and laterally to obtain passivity of flap movement and absence of muscle pull or periosteal adhesion. The flap is rotated laterally to cover the recession defect completely and extend for approximately 1 mm coronal to the cemento-enamel junction. Careful flap suturing is performed to position and secure the soft tissues over the root surface by means of sling and simple sutures (Santana et al., 2010).
Figure 1. Schematic drawing of rotational flap procedure.
Figure 2. Schematic drawing of double papilla flap technique.
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A. L. Dumitrescu, Liviu Zetu and Silvia Teslaru
Following removal of the dressing and the sutures, usually after 10-14 days, the patient is instructed to avoid mechanical tooth cleaning for further 2 weeks, but to use twice daily rinsing with chlorhexidine solution as a means of infection control (Weneström et al., 2008). Several modifications have been described to overcome the problem of dehiscence at the donor site. Staffileno (1964) used a split-thickness pedicle flap so as not to denude the adjacent site. This approach compromises vascularity and does not preclude bone resorption at the donor site (Bahat et al., 1990). Other modifications of the procedure are the oblique rotated flap (Pennel et al., 1965), the rotation flap (Patur, 1977), the double papilla flap (Cohen and Ross, 1968) (Figure 2.) and the transpositioned flap (Bahat et al., 1990). Zucchelli et al. (2010) revealead that present data do not seem to indicate the laterally moved flap is an highly predictable and effective root coverage surgical procedure. From the studies reviewed, the reported mean percentage of root coverage ranges between 34% and 82% (Smuckler,1976; Guinard and Caffesse, 1978; Espinel and Caffesse 1981; Waite, 1984; Zade and Hirani, 1985; Oles et al., 1985) and only Oles et al. (1988) reported data relating the ―percentage of complete (up to the cemento-enamel junction) root coverage‖ and the range was between 40% and 50% (Zucchelli et al., 2010). 4.1.2. Advanced Flaps Procedures Since the lining mucosa is elastic, a mucosal flap raised beyond the mucogingival junction can be stretched in coronal direction to cover exposed root surfaces. The coronally advanced flap procedure has been described by several authors (Allen and Miller Jr, 1985; Harris and Harris, 1994; Milano, 1998; Romanos et al., 1993; Wennström and Zucchelli, 1997; Bernimoulin et al., 1975). The coronally advanced flap is the first choice surgical technique when there is adequate keratinized tissue apical to the recession defect. Optimum root coverage results, good color blending of the treated area with respect to adjacent soft tissues, and recuperation of the original morphology of the soft tissues margin can be predictably accomplished using this surgical approach. Furthermore, the coronally advanced flap is very effective in treating multiple recession defects affecting adjacent teeth with obvious advantages for the patient in terms of esthetics and morbidity. Some unfavorable local anatomic conditions may render the coronally advanced flap contraindicated: 1) the absence of keratinized tissue apical to the recession defect; 2) the presence of gingival (―Stillman‖) cleft extending in alveolar mucosa; 3) the marginal insertion of frenuli; 4) the presence of deep root structure loss; or 5) presence of a very shallow vestibulum. In these situations the clinician should take the soft tissues located laterally to the recession defect into consideration to evaluate the possibility to perform a laterally moved flap (Zucchelli et al., 2010; Wennström and Zucchelli, 1996; Zucchelli and De Sanctis, 2000). The coronally positioned pedicle graft has many advantages over other surgical procedures used to cover exposed roots. It does not require a separate surgical site to obtain a graft. The tissue utilized will be a perfect color and contour match with the surrounding tissue. Additionally, the procedure is simple to perform and does not require a lot of time (Harris and Harris, 1994). In aim to evaluate the predictability of the procedure several clinical studies have been evaluated by Bouchard et al., 2001. The mean depth of the recession defects treated was 3.7 mm (3.3–4.1mm). The mean % of root coverage for advanced flaps was reported to be 77%
Aesthetic Periodontal Therapy – Root Coverage
9
(55–98), while the % of teeth with complete root coverage was 45% (9-84%) (Bouchard et al., 2001). More recently, Cairo et al. (2008) reviewed the clinical outcomes of the coronally advanced flap on a total of 794 Miller Class I and II gingival recessions in 530 patients from 25 RCTs. This systematic review confirms that the coronally advanced flap procedure is a safe and reliable approach in periodontal plastic surgery and is associated with consistent recession reduction and frequently with complete root coverage. The results of meta-analyses showed that only two combinations (coronally advanced flap + connective tissue graft and coronally advanced flap + enamel matrix derivative) provided better results than coronally advanced flap alone. Coronally advanced flap + connective tissue graft resulted in better clinical outcomes for both complete root coverage (OR=2.49) and recession reduction (10.49 mm) compared with coronally advanced flap, and no other therapy provided better results than coronally advanced flap + connective tissue graft. The combination of coronally advanced flap + enamel matrix derivative was associated with a higher probability to obtain complete root coverage (OR=3.89) and a higher amount of recession reduction (0.58 mm) than coronally advanced flap alone. A possible benefit following root coverage procedures may be the augmentation of keratinized tissue. This systematic review showed that coronally advanced flap + connective tissue graft was associated with better clinical outcomes in terms of keratinized tissue gain following therapy. The technique for the coronally advanced flap procedure is: The coronally advanced flap is initiated by two horizontal bevelled incisions (3mm in length), mesial and distal to the recession defect located at a distance from the tip of the anatomical papillae equal to the depth of the recession plus 1 mm.Two bevelled oblique, slightly divergent, incisions starting at the end of the two horizontal incisions and extending to the alveolar mucosa. The resulting trapezoidal-shaped flap is elevated with a split–full– split approach in the coronal–apical direction. In order to permit the coronal advancement of the flap, all muscle insertions present in the thickness of the flap are eliminated. This is done keeping the blade parallel to the external mucosal surface. Coronal mobilization of the flap is considered ―adequate‖ when the marginal portion of the flap was able to passively reach a level coronal to the CEJ of the tooth with the recession defect. In fact, the flap should be stable in its final coronal position even without the sutures. The root surface is mechanically treated with the use of curettes. It must be considered that only the portion of the root exposure with loss of clinical attachment (gingival recession1 probeable gingival sulcus/pocket) is instrumented. Exposed root surfaces belonging to the area of anatomic bone dehiscence were not instrumented not to damage connective tissue fibres still inserted in to the root cementum. The facial soft tissue of the anatomic inter-dental papillae coronal to the horizontal incisions is disepithelized to create connective tissue beds to which the surgical papillae of the coronally advanced flap are sutured. By moving the flap coronally to reach the tip of the disepitelized anatomical papillae, the vestibular soft tissue should be positioned 1 mm coronal to the cemento-enamel junction to account for soft tissue shrinkage. The suture of the flap is started with two interrupted periosteal sutures performed at the most apical extension of the vertical releasing incisions; then, it proceeded coronally with other interrupted sutures, each of them directed, from the flap to the adjacent buccal soft tissue, in the apical–coronal direction. This is done to facilitate the coronal displacement of the flap and to reduce the tension on the last coronal sling suture (De Sanctis and Zucchelli, 2007) (Figure 3.).
10
A. L. Dumitrescu, Liviu Zetu and Silvia Teslaru
Figure 3. Coronally advaced flap procedure. a. A recession defect on the lower canine. b. Close suturing of the pedicle graft to cover the exposed root surface. c. Healing outcome 3 months post-operatively. d. Healing outcome 1 year post-operatively.
For the treatment of isolated gingival recession, Zucchelli et al. (2004) proposed the use of a laterally moved and coronally advanced flap. Thereafter, the proposed surgical technique combined the root coverage and esthetic advantages of the coronally advanced flap with the increase in gingival thickness and in the amount of keratinized tissue associated with the use of the laterally moved flap and resulted in a very high mean percentage of root coverage (96%) and complete soft tissue root coverage (up to the CEJ) accomplished in 80% of treated cases. The main modification of the present surgical technique, with respect to those previously proposed, was the elimination of all muscle insertions in the thickness of the flap to permit the coronal advancement of the laterally moved flap. Furthermore, the coronal advancement of the flap allowed the surgical papillae to cover the anatomic papillae which represented the most coronal areas for anchoring the flap and a critical source for vascular exchanges. In addition, coronal advancement of the flap beyond the cemento-enamel junction likely compensates for the post-surgical soft tissue contraction, resulting in no exposure of the root surface (Zucchelli et al., 2004). The different thickness during flap elevation (greater in the central area than in the more peripherical portions of the flap) represented another aspect of the proposed surgical technique. In a thicker flap the amount of vascularized connective tissue increases and the post-surgical soft tissue contraction decreases. Both these factors improve the possibility of accomplishing and maintaining root coverage (Zucchelli et al., 2004).
Aesthetic Periodontal Therapy – Root Coverage
11
Another feature of the present surgical technique was the sequence of sutures: the apical stabilization sutures in the most apical extension and along the releasing incision and the double mattress horizontal suture at the fornix were performed before the marginal sling suture. Thus the most marginal portion of the flap was stable in the desired coronal position without disrupting forces acting on it at the time of the final suture. Furthermore the double mattress suture reduced lip tension on the marginal portion of the flap during the first healing period and avoided the use of surgical periodontal dressing (Zucchelli et al., 2004).
The Semilunar Flap The coronally positioned flap may be preferable in situations with multiple recession defects. In situations with only shallow defect the semilunar coronally positioned flap described by Tarnow (1986) offers an alternative approach. The semilunar coronally repositioned flap has the following advantages: (1) there is no tension on the flap after coronally repositioning it; (2) there is no shortening of the vestibule; (3) the papillae mesial and distal to the toothbeing treated remain cosmetically unchanged; (4) no sutures are needed because the lack of tension of the tissue being coronally positioned (Tarnow, 1986). The technique for the semilunar coronally repositioned is: A semilunar incision is placed apically to the recession and at a distance from the soft tissue margin, which should be approximately 3 mm greater than the depth of the recession (Figure 4.). The outline of the incision should be parallel to the curvature of the gingival margin. The incision is extended into the papilla region on each side of the tooth, but care should be taken to secure a collateral blood supply to the pedicle graft. A split thickness dissection of the facially located tissue is then made by an intracrevicular incision extending apically to the level of the semilunar incision. The mid-facial soft tissue graft is coronally repositioned to the level of the cemento-enamel junction and stabilized by light pressure for 5 min.No suturing is needed but a light curing dressing is applied for wound protection (Wennström and Pini Prato, 1997).
Figure 4. Schematic drawing of semilunar coronally repositioned flap.
12
A. L. Dumitrescu, Liviu Zetu and Silvia Teslaru
Despite the lack of tension in the mobilized pedicle, its stability in the more desired coronal position is questionable, as no suturing of the advanced flap portion is indicated. This is of particular concern when the procedure is considered for teeth with highly scalloped gingival margins, where coronally manipulating the tissue could be more demanding (Haghighat, 2006). The semilunar flap is a modification of a technique described in the late 1960s for incisally repositioning the gingival tissues to address recession defects on labial surfaces of maxillary cuspids (Sumer, 1969; Haghighat, 2006). In a in a split-mouth design the outcome of gingival recession therapy using subepithelial connective tissue graft or the semilunar coronally positioned flap procedure was evaluated by Bittencourt et al. (2006). No statistically significant differences were observed between groups in any of the clinical parameters at baseline. Recession height, recession width, width of keratinized tissue, thickness of keratinized tissue, probing depth, and clinical attachment level were measured at baseline and 6 months post-surgery. In the subepithelial connective tissue graft group, recession height decreased from 2.20 ± 0.56 mm to 0.21 ± 0.25 mm, corresponding to a mean root coverage of 90.95% ± 11.46%. In the semilunar coronally positioned flap group, recession height decreased from 2.15 ± 0.59 mm to 0.10 ± 0.19 mm, corresponding to a mean root coverage of 96.10% ± 7.69. Complete root coverage was accomplished in 52.94% of the treated cases in the subepithelial connective tissue graft group and in 76.47% in the semilunar coronally positioned flap group (Bittencourt et al., 2006). After 30 months, the mean percentages of root coverage were 89.25% and 96.83% for the semilunar coronally positioned flap and subepithelial connective tissue graft groups, respectively. Complete root coverage at the final observation was achieved in 58.82% of the treated cases in the semilunar coronally positioned flap group and in 88.24% of the patients in the subepithelial connective tissue graft group. The comparison between 6 and 30 months showed that two patients in the subepithelial connective tissue graft group gained attachment and achieved complete root coverage; this only occurred in one patient in the semilunar coronally positioned flap group. The subepithelial connective tissue graft group maintained a statistically significant increase in thickness of keratinized tissue (P 5 mm > 6 mm severe erythema severe oedema and ulcers spontaneous bleeding
II
absent
slight, perivascular and scattered intraepithelial
mild, continuous in the lamina propria and intraepithelial
DE
normal epithelium
outer layer shedding
outer layer shedding cell swelling
severe, continuous in the lamina propria and dense intraepithelial as in # 2, plus ulceration
PMN, MN, RBC DEC
absent
10
normal
aberrant shape
plasma membrane rupture vacuolation
conglutination, vacuolation cell debris
absent
< 10
10-30
> 30
cocci, bacilli, spirochetes
CAL, clinical attachment level; PD, probing depth; GI, gingival index; II, inflammatory infiltrate; DE, damaged epithelium; PMN, polymorphonuclear leukocytes; MN, mononuclear leukocytes; RBC, erythrocytes; DEC, damaged epithelial cells.
Table 2. Severity scoring of periodontitis Clinical score
Bioptic score
Cytodiagnostic fluorescence score
Case No. CAL
PD
GI
Total score
II
DE
Total score
PMN
MN
RBC
DEC
Cocci
Bacilli
Spiro-chete
1
1
2
1
4
2
1
3
2
1
0
0
1
1
0
2
1
1
0
2
0
0
0
0
0
0
0
0
2
0
3
3
3
2
8
3
1
4
1
3
0
1
1
0
0
4
2
2
2
6
2
2
4
2
2
3
0
1
1
0
5
3
3
3
9
3
3
6
3
3
1
3
1
2
3
6
3
3
3
9
3
3
6
3
3
2
3
1
2
1
7
3
3
3
9
3
3
6
3
3
1
1
1
1
1
8
3
3
3
9
3
3
6
3
3
2
3
3
2
1
9
3
2
0
5
2
1
3
1
2
0
1
2
2
0
10
2
1
0
3
2
1
3
1
2
0
1
2
1
0
11
2
2
3
7
3
3
6
3
1
3
2
3
3
3
12
1
1
0
2
2
0
2
0
2
0
0
2
0
0
13
2
2
0
4
2
1
3
1
2
0
1
2
0
0
14
1
2
0
3
1
1
2
1
1
0
1
2
1
0
15
2
3
3
8
3
3
6
3
1
2
3
1
3
1
Table 2. (Continued) Clinical score
Bioptic score
Cytodiagnostic fluorescence score
Case No. CAL
PD
GI
Total score
II
DE
Total score
PMN
MN
RBC
DEC
Cocci
Bacilli
Spiro-chete
16
2
2
3
7
3
3
6
3
1
3
3
1
1
3
17
3
3
0
6
3
1
4
1
3
0
0
2
2
1
18
3
2
1
6
2
1
4
1
2
0
1
2
2
0
19
3
1
0
4
0
0
0
0
0
0
0
3
0
0
20
2
2
3
7
3
3
6
3
1
2
3
1
3
2
21
2
2
2
6
3
3
6
3
3
1
3
3
0
0
CAL, clinical attachment level; PD, probing depth; GI, gingival index; II, inflammatory infiltrate; DE, damaged epithelium; PMN, polymorphonuclear leukocytes; MN, mononuclear leukocytes; RBC, erythrocytes; DEC, damaged epithelial cells.
Novel Cytodiagnostic Fluorescence Assay for the Diagnosis…
143
Table 3. Spearman’s non-parametric correlation test
Clinical score
vs. II (biopsy) PMN MN RBC EDC cocci bacilli spirochetes
r 0.7670 0.8327 0.5248 0.6131 0.6993 -0.07588 0.4263 0.6012
r squared 0.5882 Gaussian approx. 0.2754 0.3759 0.489 0.005758 0.1817 0.3615
p value 60 years, diabetes, poor glycaemic control, obesity, macroalbuminuria, smoking, high serum level of CRP, elevated total cholesterol, low levels of high-density lipoprotein (HDL) cholesterol, race/ethnicity, gender and income/poverty; non-traditional risk factors that may contribute to CKD include periodontal disease and instruction level [171, 172]. The effects of CKD on oral tissues, especially in children, including xerostomia, delayed tooth eruption, calcifications leading to obliteration of pulp chamber and canals, enamel hypoplasia, decreased caries rates and altered salivary pH levels are well-documented [173]. Besides in patients with CKD receiving haemodialysis it is characteristic the malodor or ‗bad breath‘ and a metallic taste which are due to the high urea content in saliva and its subsequent breakdownto ammonia[174]. Dental management in CKD patients is complicated by some systemic consequences (e.g. anaemia, crisis of bleeding and cardiovascular or endocrine diseases). Moreover, untreated dental infection in immune-suppressed individuals can potentially contribute to morbidity and transplant rejection[175]. For this reason, many transplant centres plan a dental check in their pre-transplant protocol. Specific effects of CKD and renal replacement therapy on periodontal tissues include gingival overgrowth and increased gingival inflammation[176]. Recent studies suggest
that chronic periodontitis may contribute to the overall chronic systemic inflammatory burden and therefore may have consequences in the management of end-stage renal disease in patients on haemodialysis or maintenance therapy[23, 177]. Interventional studies are needed to assess the effect of periodontal treatment on systemic inflammation and CKD patients in this population.
Periodontal Disease and Osteoporosis Osteoporosis (OP) is a systemic skeletal disease characterized by low bone mass and micro-architectural deterioration of bone tissue, with a consequent increase in fragility and susceptibility to fracture of bones[178]. In the past, OP was considered a physiological
232
Giuseppe Pizzo, Rosario Guiglia and Giuseppina Campisi
process associated with ageing, but today it is viewed as a heterogeneous chronic systemic condition which can occur in any age and its aetiology is attributed to various endocrine, metabolic and individual factors.Furthermore, recently OP has received increasing attention in relation to the susceptibility to PD in postmenopausal women[179, 180]. The production of estrogens changes drastically at menopause leading to OP in skeletal bones characterized by the loss of bone mass and reduction of bone density with a consequent increase in bone fragility and susceptibility to fracture. Total skeletal mass reduction in postmenopausal women may include jawbones, particularly the mandible[181]. A number of studies showed that bone changes in OP are associated with loss of periodontal attachment, loss of teeth, and height of residual ridge [182, 183]and an hypothesis of a bi-directional aetiological mechanism has been advanced.In the presence of severe generalized OP, reduced bone mineral density implies an increased porosity of the alveolar bone at the jaw bone, an altered trabecular pattern and a more rapid bone resorption in presence of chronic periodontitis Furthermore, bacteria, directly through the release of toxins, or indirectly through the release of inflammatory mediators, alter the normal homeostasis of bone tissue, increasing osteoclastic activity and reducing bone density [19]. The loss of bone mass that is observed in these two conditions appears to be modulated by systemic and local factors, sometimes common, as are many risk factors (Table 3). However, a definitive evidence is lacking. Table 3. The risk factors for osteoporosis and periodontal disease Risk Factors For Osteoporosis Common Risk Factors Systemic Risk Factors Systemic Risk Factors - Female gender - Ageing - Low body weight/stature/very thin body - Gender - Premature menopause (