The Australian Journal of Periodontology and Implant Dentistry Limited

Transcription

1 VOLUME 1 Issue 1 June 2017 A O S and Implant Dentistry Limited The Official Journal of the Australian Society of Periodontology and the Australasian Osseointegration Society IN THIS ISSUE The Effectiveness of Azithromycin in Periodontitis and Peri-implantitis Colonisation of the Oral Cavity: Birth to Late Teenage Years Dental Implant Screw Mechanics Australian Periodontology Research Foundation (APRF) News ASP & AOS State Branch News A O S Australasian Osseointegration Society limite ed

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3 VOLUME 1 Issue 1 June 2017 Contents A Authors Guidelines 2 Editor s Notes 3 President s Notes 4 The Effectiveness of Azithromycin in Periodontitis and Peri-implantitis Colonisation of the Oral Cavity: Birth to Late Teenage Years Dental Implant Screw Mechanics 27 Australian Periodontology Research Foundation (APRF) News ASP & AOS State Branch News Editor Professor Ivan Darby Periodontics Melbourne Dental School University of Melbourne 720 Swanston Street PARKVILLE VIC 3010 Australia editor@ajpid.org.au Editorial Board Dr Fritz Heitz, Western Australia Prof. Saso Ivanovski, Queensland Prof. Iven Klineberg, New South Wales Dr George Pal, New South Wales Dr Simon Watson, Victoria How to reach us: Paper submission & letters to the editor editor@ajpid.org.au Journal annual subscription (for non-members) admin@ajpid.org.au ASP Membership enquiries contact@asp.asn.au AOS Membership enquiries info@aos.org.au Journal enquiries admin@ajpid.org.au Journal Compilation Lisa Sullivan 1

4 A VOLUME 1 Issue 1 June 2017 Authors Guidelines Submissions welcome! Australian Journal of Periodontology and Implant Dentistry aims to promote the field of Periodontics and Implant Dentistry through clinical papers, original research, review articles, case reports and other correspondence that the Editor thinks appropriate to print. Submissions of articles covering these areas are welcomed. Contributions should be submitted in electronic form (preferably in Microsoft Word) by to the editor. The contribution should be prepared with double spacing and 2.5 cm margins. A letter signed by all its authors must accompany an article. The author s name should appear under the title and the full postal address at the end of the text. Clinical and original research papers should be clearly divided into Abstract, Introduction, Materials and Methods, Results and Discussion. All manuscripts will be sent to a reviewer for assessment. Tables, figures, photographs and radiographs should be submitted either contained in the Word file or in separately clearly labeled files. References should be set out in the Uniform Requirement (Vancouver) style. Identify references in the text, tables and legends by the first author s name and the year of publication, in parentheses. A list of references should be provided in alphabetical order at the end of the manuscript. If the reported research involves either human or animal experimentation then the authors must indicate that the ethical guidelines of the Australian National Health and Medical Research Council or the Declaration of Helsinki have been applied. If the research involves human subjects then the authors must state that informed consent was obtained. Material is received on the understanding that it may be subject to Editorial revision and that, on acceptance, becomes the property of the Australian Journal of Periodontology and Implant Dentistry. All expressions of opinion or statements of supposed facts are those of the authors and are not to be regarded as the views of the ASP/AOS or Editorial Board of Australian Journal of Periodontology and Implant Dentistry. Subscription All members of the Australian Society of Periodontology and the Australasian Osseointegration Society will receive two publications per year as part of their membership. The annual subscription for 2017 will be $68.00 plus $10.00 postage & handling plus GST within Australia & A$68.00 plus A$20.00 for overseas postage and handling. Order queries should be sent to the AJPID Administrator Kayla Ashkar: admin@ajpid.org.au 2

5 VOLUME 1 Issue 1 June 2017 Editor s Notes A Welcome Welcome to the first edition of the Australian Journal of Periodontology and Implant Dentistry and welcome to members of the Australasian Osseointegration Society. The journal has resulted from discussions between the Presidents of the ASP & AOS. Based on Periodontology it expands the scope adding articles on restorative implant dentistry to periodontics and surgical implant dentistry. However, it will still have the same layout and include local branch news and Australian Periodontal Research Foundation updates. As with any journal, we rely on articles to be submitted and welcome papers covering the aforementioned topics. In this edition there are three articles. The first discusses the use of azithromycin as an adjunct to periodontal and implant treatment. Azithromycin is currently in fashion and can work well in the management of aggressive periodontitis. However, the scientific evidence for its use is somewhat lacking. The second article looks at the colonisation of the oral cavity from birth by the microflora. As you are no doubt aware we get our bacteria from our parents, but the species or strains you get as a child/teenager may affect your chances of getting periodontal disease later in life. The last article reviews implant screw mechanics and management of fractures. My understanding is that these are one of the most frequent technical complications and the paper provides an overview of how to reduce the incidence. As ever, I hope you enjoy the articles. Prof. Ivan Darby 3

6 A VOLUME 1 Issue 1 June 2017 President s Notes On behalf of the Australian Society of Periodontology (ASP) and the Australasian Osseointegration Society (AOS) we are delighte d to introduce the first issue of the new Australian Journal of Periodontology and Implant Dentistry (AJPID). This joint publication represents a collaboration that brings together the interdisciplinary readership of the societies, and promises to enhance the natural knowledge synergy between the ASP and AOS. The genesis of the AJPID was pursued by Prof Saso Ivanovski and Dr George Pal, as the recent past presidents of the ASP and AOS, with Prof Ivan Darby as an indispensible guide through the process of generating a new journal from the existing ASP publication: Periodontology. As the longstanding editor of Periodontology, Prof Darby was ideal to continue to steer the new AJPID. The bi-annual journal aims to present at least three articles per issue, updates on the State branches and Federal activities of each of our societies, and an update from the Australian Periodontology Research Foundation. The journal will also include advertising from our generous sponsors, without which, producing this journal would not be possible. The new journal committee includes our editor Professor Ivan Darby, Dr Fritz Heitz and Professor Saso Ivanovski representing the ASP, Drs Simon Watson and George Pal representing the AOS and support staff Ms Kayla Ashkar and Ms Lisa Sullivan. We are pleased that Professor Iven Klineberg has accepted our invitation to join the Editorial Board. A webpage for the journal can be found at For the ASP, we would like to thank the immediate past ASP President Saso Ivanovski, Treasurer Ryan Lee, and the ASP federal council for their tireless work managing the affairs of the society, and in particular a very successful Biennial meeting in Brisbane. Planning for the next Biennial meeting is progressing well. The conference will be held in Perth from 8-10 March, The theme of the meeting is Perio Power how dentistry can profit from periodontics. We have already secured a number of international keynote speakers in Professor Björn Klinge (University of Malmö and Past President of the European Association of Osseointegration), Professor Gianni Salvi (University of Bern) and Dr Jeanie Suvan (Eastman Dental Institute, University College London). The AOS has an exciting year ahead. With the support of the Federal branch, Professor Tord Berglundh will be lecturing to the QLD, NSW, VIC and WA branches in October. The AOS biennial conference will be held 3-5th May, 2018 in Melbourne, under the theme of Planning today for tomorrow s success. Already we have secured a great international speaker line-up including; Prof Tomas Albrektsson (Sweden), Prof Irena Sailor (Switzerland), Clin Prof Frank Schwarz (Germany) and Assoc Prof Stefan Fickl (Germany), with more to be announced soon, together with a great complement of highly regarded local speakers. So save these dates and check for programming updates and registration details on the conference website, More details for each of the State branches events and the upcoming conference can be found elsewhere in the journal, and details will be updated in future editions, or visit the AOS website We hope you enjoy this first issue, and issues to come, of Australian Journal of Periodontology and Implant Dentistry. Dr Fritz Heitz ASP Federal President Dr Simon Watson AOS Federal President 4

7 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited The Effectiveness of Azithromycin in Periodontitis and Peri-implantitis Gabriel Rodriguez-Ortiz Introduction Periodontitis is an infectious disease of the host caused by the activities of specific periodontal pathogens that provoke the disease process. However, it is the quality and nature of host responses of the pathogen that may control much of the pathology. It is characterized by the occurrence of an irreversible destruction of periodontal supporting tissue that occurs over an extended period of time (Kornman et al, 2008). The complex structure of the periodontal biofilm, consisting of multiple bacterial communities residing in a glycocalyx matrix, has been well described by Marsh et al (2005). It has been demonstrated that once bacteria attach to a tooth surface and reside within a mature biofilm structure they have a reduced susceptibility to antimicrobials compared to planktonic or free floating bacteria. Therefore, mechanical debridement is considered crucial to disrupt the biofilm when using systemic antibiotics to treat periodontitis (Heitz- Mayfield, 2009). It has also been well documented that the majority of patients diagnosed with periodontitis can be successfully treated following mechanical debridement, adequate oral hygiene and regular maintenance care (Axelsson, 1981). Although it has been shown that bacterial species residing in biofilms are much more resistant to antibiotics than the same species in a planktonic state (Brown 1988, Hoyle 1990), antibiotics have been used frequently in the treatment of periodontal infections. The rationale for use of adjunctive systemic antimicrobials is to further reduce the bacterial load enabling resolution of the inflammation in the periodontal pocket. Herrera et al (2002), indicated that systemic antibiotics used in conjunction with scaling and root planing can offer an additional benefit over scaling and root planing alone in terms of probing depth reduction and clinical attachment level gain in pockets of 6 mm or deeper. Similar findings were reported in the systematic review by Haffajee et al (2003). The range of antibiotics used to treat periodontal infections is quite extensive. Antibiotics including the tetracyclines, metronidazole and the combination of MET and amoxicillin Abstract: Azithromycin is a macrolide antibiotic extensively used as an adjunct to mechanical debridement in the treatment of periodontitis. The short dosage regime of this agent and the long life in serum and periodontal tissues has increased its popularity in recent years. Although a number of studies that have evaluated the efficacy of azithromycin it s use is controversial in periodontitis and scarce in peri-implantitis. Based on this debate, this paper discusses the evidence for the effectiveness of Azithromycin in periodontitis and periimplantitis by reviewing the clinical and microbiological parameters of the most cited studies. Although some authors have demonstrated certain benefits when azithromycin was used, particularly in aggressive periodontitis and in smokers, others could not show enough evidence to support its use in the treatment of periodontal diseases. It is also concluded that although periodontal health was achieved in aggressive and chronic periodontitis. The antibiotic did not show major effects on the subgingival microflora over scaling and root planing alone, particularly 12 months after administration. Periimplant inflammation reduced in patients treated with azithromycin. Keywords: Antibiotics, Azithromycin, periodontitis, peri-implantitis, scaling and root planing, periodontal pathogens, randomized control trial, systemic antibiotics, chronic periodontitis, aggressive periodontitis 5

8 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited have been the most commonly used agents to treat different forms of periodontitis. Other systemic drugs have been used with fewer studies. Of those, Azithromycin is becoming a well accepted drug as an adjunctive to periodontal therapy as it has short dosage regime that improves patient compliance and has limited side effects, which is considered a major problem of several antibiotic protocols, such as metronidazole and metronidazole + amoxicillin (Gerrero et al, 2005). However, as Feres et al (2015) indicated, the results of the few randomized clinical trials that have evaluated the effects of azithromycin in periodontal treatment are somehow controversial (Smith 2002, Dastor 2007, Emingil 2012, Gomi 2007, Haas 2008, Haffajee 2007, Han 2012, Mascarenhas 2005, Oteo 2010, Sampaio 2011, Yashima 209) (See Table 1). Although some authors demonstrated certain benefits when azithromycin was used as an adjunct to mechanical debridement in the treatment of aggressive periodontitis (Haas, 2008), smokers (Mascarenhas, 2005) or in cases of mild/moderate chronic periodontitis (Haffajee, 2007; Oteo, 2010, Smith, 2002), others could not show a benefit (Emingil, 2012; Han, 2012, Sampaio, 2011). Azithromycin Azithromycin is a wide-spectrum bacteriostatic macrolide with in vitro activity against aerobic and anaerobic gramnegative microorganism (Retsema et al. 1987), and emerged as a promising drug in medicine in the early 1990s and more recently in dentistry (Smith 2002, Mascarenhas 2005, Haas 2008, Haffajee 2007, Oteo 2010, Yashima 2009). Azithromycin presents good pharmacological properties, such as rapid absorption, high tissue concentration (Hoepelman, 1995) and long half-life in human serum and periodontal tissues. Data have shown that Azithromycin concentrations in gingival fluid (GCF) are higher and more sustained than in serum (Lai et al. 2011). Azithromycin is detectable in inflamed periodontal tissues >14 days after systemic administration (Gomi et al. 2007a; Gladue, 1898, 1990), allowing oncedaily dosing (500 mg) for 3 6 days (Henry, 2003). Azithromycin is found in high concentrations in fibroblasts and phagocytes (McDonald & Pruul 1991) and is carried to areas of inflammation as a result of chemotactic effects exerted on the phagocytes (Schentag & Ballow 1991), thus targeting the drug at those sites. Different in vitro (Pajukanta 1993) and in vivo (Herrera et al. 2000) studies have demonstrated the efficacy of azithromycin against P. gingivalis. Only few side effects have been reported with the use of Azithromycin, such as cardiotoxicity and gastro intestinal upset. Most data on the occurrence of cardiotoxicity has been presented in case studies and which shows a prolongation of the QT interval and Torsades de pointes (TdP). TdP is a rare polymorphic ventricular tachycardia, usually following QT prolongation, which is caused by altered cardiac repolarization and is usually associated with syncope, but may result in death (Owens, 2004). Although there have been reports associating azithromycin with the development of TdP, it seems that most occurrences are associated with erythromycin, and as such azithromycin is considered a low risk drug (Owens, 2004). Ray et al in 2012 in an observational study raised the attention focused on the cardiotoxicity of azithromycin in the popular media. Results from this study showed that patients with known cardiac disease were at an increased risk of cardiovascular death, following a 5 day course of azithromycin. However a clear limitation of this study was the fact that it was an observational study, which makes interpreting the results difficult. Efficacy of Azithromycin in periodontal disease In the first clinical report of azithromycin as an adjunctive to non-surgical therapy in the treatment of periodontitis, Smith et al. (2002) treated 46 patients either with the antimicrobial, 500 mg azithromycin once a day for 3 days or placebo, administered 2 weeks after the commencement of oral hygiene instructions and mechanical debridement. Results of the study showed that by week 22 the percentage of pockets that had remained deeper than 5 mm in the azithromycin group was significantly less (5.6%) compared to the placebo group (23.3%). Additionally it was found that for pockets, which were initially deeper than 4 mm, the test group had less sites 3 mm (21.6%) after 22 weeks than the control group (44.3%). The other parameters, which were also found to be favourable for azithromycin, were fewer pockets failing to improve in probing depth (Azithromycin, 6.6%; vs Placebo, 21.6%) and fewer continuing to bleed on probing (Azithromycin, 46.9%; vs Placebo, 55.6%). Pocket depths initially measured at 4 to 5 mm or 6 to 9 mm also showed lower mean pocket depths in the patients on azithromycin at weeks 6, 10 and 22, with all measurement reaching statistical significance. Based in those results it is concluded by Smith et al, that the greatest benefits of adjunctive azithromycin therapy will be in deeper pockets. In addition, the results of this study demonstrate both statistically significant and 6

9 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited Table 1: Group of studies showing benefits of AZM in periodontal therapy. Modified from Hirsh et al (2012) Author/year Type Case No Test/Cont Smith, 2012 Mascarenhas, 2005 Haffajee, 2007 Oteo, 2010 Haas, 2012 Gomi, 2007 Yashima, 2009 Dastor, 2007 R, DB, PC Intervention 23/21 T:SRP+AZM C:SRP+Placebo R, SB 15/15 T:SRP+AZM C:SRP R, SB 25/23 T:SRP+AZM C:SRP R, DB, PC 15/13 T:SRP+AZM C:SRP+Placebo RCT 12/12 T:SRP+AZM C:SRP+Placebo R 17/17 T:SRP+AZM C:SRP R, DB 10/10 T:SRP+AZM C:SRP RCT 15/15 T:SRP+AZM C:SRP A All had periodontal surgery with osseous contouring after initial SRP; all subjects were given 600 mg of ibuprofen after surgery.+placebo Follow up time 0, 1, 2, 3, 6, 10, 22 weeks Summary PD s initially 4 5 mm or 6 9 mm showed significantly more depth reduction in patients on AZM, at weeks 6, 10 and 22. 3, 6 mo AZM group showed enhanced reductions in PD s and gains in CAL at moderate (4 6 mm) and deep (>6mm) sites. Favorable changes in in microflora in AZM group 3, 6, 12 mo Greater PD reduction and greater CAL gain in sites with pockets > 6 mm initially for AZM and MET groups for up to 12 mo. AZM reduced levels of T forsythia for up to 12 mo, 1, 3, 6 mo Greater PD reductions, CA gains, decreased A. a, P. intermedia, T. forsythia and P. micra after 1, 3 and 6 mo in AZM group. 5, 13, 25 weeks 1, 3, 6, 9, 12 mo Greater PD reductions, CA gain in AZM group for up to 12 mo. Greater reductions in mean PD, number of bleeding on probing sites and GCF levels at 13 and 25 wk. Greater PD reductions, CA gain, number of BOP, GI in AZM group for up to 12 mo. Sustained reduction in periodontal pathogens in AZM group. No significant difference was found for BOP, PD or CAL between both groups Comments Short study, uncertain whether controlled for smoking Beneficial effect of AZM shown in smokers Study not controlled for smoking. Severity/diagnosis of periodontitis at baseline difficult to assess. Study was not placebo controlled Small number of subjects further compromised by including both smokers and nonsmokers Five smokers out of 24 subjects. Study not properly controlled for smoking status Short study, not properly controlled Different treatments for test and control groups make results difficult to compare Only study of effects of AZM after periodontal surgery; cannot compare with other studies AZM, azithromycin; CAL, clinical attachment loss; FM-SRP, full mouth SRP single visit; GCF, gingival crevicular fluid; MET, metronidazole; RCT, randomized controlled trial; SDD, sub-antimicrobial doxycycline; SRP, scaling and root planing; R, randomized; DB, double blinded; PC, placebo controlled. 7

10 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited clinically relevant benefits of adjunctive azithromycin in the treatment of advanced periodontitis in adult patients. The results of the microbiology analysis of Smith s paper were previously reported by Sefton et al (1996). The authors found that there were significantly less black-pigmented anaerobes and spirochetes 6 weeks after azithromycin administration compared to the control. Microbiological counts at 22 weeks showed that although there were still significantly less spirochetes in the test group compared to control, there was not a statistical difference between the groups in relation to black pigmented anaerobes. In a randomized, single-masked, controlled clinical trial study, Mascarenhas et al (2005), determined whether the use of azithromycin improves the outcomes obtained in combination with non-surgical periodontal treatment in smokers. The study was done in 31 smokers, treatment consisted of SRP and AZM in the test group and only SRP in the control group. The results demonstrated that both groups displayed clinical improvements in PD and CAL that were sustained for 6 months. However, patients treated with SRP + AZM showed enhanced reductions in PD and gains in CAL at moderate (4 to 6 mm) and deep sites ( 6 mm) (P < 0.05). Furthermore, patients of Mascarenhas study were subject to the BANA test, which determines the proteolityc activity of anaerobic bacterias (Porphyromonas gingivalis, Treponema denticola, and Bacteroides forsythus - red complex). The group of patients that had SRP + AZM resulted in greater reductions in BANA levels compared to SRP alone (P < 0.05) while rebounds in BANA levels were noted in control group at the 6-month evaluation. The reduction in the percent of BANA positive sites from baseline to 6 months was about 10-fold higher for the test group. Although AZM helped to reduce microorganisms from baseline to 6 months, a trend of bacterial recolonization was noted in both groups. Similar reductions in black pigmented anaerobes were confirmed in others studies (Haffajee et al., 2007, Gomi et al., 2007) although it was found that instead of a true reduction in total bacterial numbers, the reductions in black pigmented anaerobes rather represented a significant shift in the bacterial ecology (Gomi et al., 2007). The long term clinical significance of these findings is also not clear, as it was found that, although an initial difference in bacterial profile was present between subjects who had taken azithromycin compared to those who did not, there was no statistically significant difference after 12 months (Haffajee et al., 2007). This is in agreement with Slots et al (1979), who showed that a single episode of periodontal treatment including antibiotics immediately decreased the total number of subgingival organisms by 10- to 100-fold. However, several Gram-negative anaerobic species returned to pre-treatment proportions after 3 to 6 months. These outcomes were further confirmed by other investigations (Lavanchy et al 1987, Sbordone et al 1990). This observation may indicate that, in order to achieve long-standing microbiological and clinical results, re-administration of antibiotic may be needed every 6 months. Clinical improvements were also noted in other studies. For instance, Haffajee et al (2007), assessed 96 patients over a one year period for gingival redness, bleeding on probing (BOP), suppuration, pocket depth (PD) and clinical attachment level (CAL). Patients were divided into 4 groups; namely scaling and root planning (SRP) only, SRP with 500 mg azithromycin once daily for 3 days, metronidazole 250 mg t.i.d. for 14 days or 20 mg doxycycline (SDD) for 3 months. Results showed that in general, patients receiving adjunct treatment exhibited greater clinical improvement compared to the SRP control, with the highest reduction in CAL found in the metronidazole group. It was found that subjects with deeper pockets (>6 mm) showed statistically significant greater pocket reductions in the azithromycin and metronidazole groups, that maintained a statistically significant difference after 12 months. The results in the study show that although metronidazole and azithromycin as adjuncts resulted in the biggest reduction in PD, metronidazole and SDD performed best in terms of CAL. As such the only reasonable explanation for the difference between PD and AL observed is that patients receiving azithromycin generally had more recession compared to the other groups. However, the results obtained in this study showed only modest improvements in clinical parameters beyond that achieved by SRP alone. The major reason for this finding was that although subjects entering the study had at least eight sites with PD >4 mm, the mean PD and AL values were quite low, suggesting that most of the subjects had mild to moderate levels of periodontitis. This is in agreement with the systematic reviews by Haffajee et al (2003) and Herrera et al (2002), in which evaluating the effects of systemically administered antibiotics suggested that antibiotics provided greater benefit in subjects with more periodontal disease and at deeper periodontal sites. More recently, a further study was conducted on patients with moderate chronic periodontitis harbouring P. gingivalis (Oteo et al., 2010). In this blinded randomised placebo 8

11 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited controlled study, patients received mechanical subgingival debridement over the course of 2 visits within a 7-day period with adjunctive azithromycin administered (500 mg for 3 days) at the last visit. It was found that the test group had significantly better improvements in terms of CAL and PPD. In terms of microbiological parameters, it was also noted that in the test group P. gingivalis decreased significantly after 1, 3 and 6 months, as did other pathogens such as T. forsythia and A. actinomycetemcomitans. However, several patients were lost to follow up over the 6-month duration of the study, there were only 15 patients available for follow up in the test group and 11 in the control group. Furthermore, the effect of smoking in the results could not be properly assessed and results from this study should be interpreted with caution. Azithromycin In Aggressive Periodontitis Few RCT studies have been conducted to evaluate the effect of adjunctive systemic antibiotics in the treatment of aggressive periodontitis (AgP) (Albandar et al 2002; Tinoco et al. 1998). Perhaps one of the reasons for this scarcity of studies is the low prevalence of AgP (Albandar 2002 & Tinoco 2002) and the consequent difficulty in recruiting cases. Furthermore, often AgP patients are not suitable to treatment, this is because the condition was diagnosed at an advanced stage of the disease, at which time the prognosis for non-surgical treatment may not be favourable. Early studies have used tetracycline and found significantly higher clinical improvement compared to controls (Palmer et al. 1996, Slots & Rosling 1983). Other studies have used doxycycline or metronidazole (Saxen & Asikainen 1993) with only small increase in crestal bone compared to placebo. Tinoco et al (1998), used a combination of Metronidazole and Amoxicillin to treat Ag Perio and reported PPD reduction of 74% and 35% of the sites showing CAL gain of 2mm, compared to 41% and 16% respectively. In a randomized controlled trial study, Haas et al in 2008, assessed the effect of adjunctive use of azithromycin with non-surgical treatment of young subjects with AgP. SRP combined with a 3-day regimen of azithromycin resulted in significant better clinical outcome parameters, including 81% PPD reduction and 51% CAL gain of 2mm, compared to SRP. This was probably the first study showing the clinical efficacy of azithromycin 1 year following non-surgical treatment of AgP in young individuals. The results also suggested that the adjunctive use of azithromycin has the potential to improve periodontal health of young patients with AgP. In addition, the effect of azithromycin is somewhat similar to the use of a combination of metronidazole and amoxicillin. In a subsequent study by Haas et al (2012), the authors compared the subgingival microbiological outcomes of azithromycin or placebo as adjuncts to scaling and root planing (SRP) in the treatment of aggressive periodontitis (AgP). In this randomized clinical trial, twenty-four AgP subjects had subgingival samples taken at baseline, after SRP and at 3, 6 and 12 months following SRP. Microbiological analysis was performed by the checkerboard DNA DNA hybridization. Although this study consisted of a small study population (n=24), the results of this study were confronting as they showed that the use azithromycin as an adjunctive to treat young subjects with AgP was ineffective in lowering the subgingival levels of important putative periodontal pathogens when compared to placebo. Although periodontal health was achieved in AgP patients treated with azithromycin, the antibiotic did not show major effects on the subgingival microflora over scaling and root planing alone in the treatment of this disease. Azithromycin vs Metronidazole + Amoxicillin in periodontitis An extensive amount of data has been presented on the beneficial effects of metronidazole or metronidazole + amoxicillin in the treatment of advanced periodontitis, the question that arises is whether azithromycin would achieve the same outcomes as either one of these two antibiotic protocols. In a study by Sampaio et al (2011), subjects were treated by azithromycin 500 mg a day for 5 days or metronidazole and amoxicillin were given three times daily for 14 days, at a dose of 400 mg and 500 mg, respectively. They received clinical and microbiological monitoring and periodontal maintenance at 3 and 6 months as well as at 1 year posttreatment. The mean baseline probing depth and clinical attachment level was, respectively, 4.8 mm and 5.3 mm for the scaling and root planing group, 4.7 mm and 5.3 mm for the azithromycin group and 4.7 mm and 5.1 mm for the metronidazole + amoxicillin group. No statistically significant differences were observed among groups at baseline for any clinical parameter (P > 0.05, data not shown). The subjects selected for this analysis presented very high mean probing depth values. As a result of this specific clinical profile, the mean number of sites with probing depth 5 mm in these subjects was much higher (approximately 60 sites) 9

12 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited than that observed in subjects from the previous analysis (approximately 40 sites). At 1 year post-treatment, subjects treated with scaling and root planing only presented a much higher mean number of sites with probing depth 5 mm (n = 29) than did those treated with adjunctive metronidazole + amoxicillin (n = 9.6; P < 0.05). The mean number of these residual sites for subjects who took azithromycin was in between (n = 19.1), but did not differ significantly from the numbers in the other two groups (P > 0.05). These results indicate an advantage of treatment with metronidazole + amoxicillin over treatment with azithromycin, which was reinforced by the data presented for changes from baseline to 1 year in probing depth and clinical attachment in initially intermediate and deep sites. (see Table 2) Only the metronidazole + amoxicillin-treated group showed statistically significantly greater reduction in probing depth and gain in clinical attachment than the group treated with scaling and root planing only. Furthermore, the adjunctive use of metronidazole + amoxicillin resulted in a more profound beneficial change in the subgingival microbial profile than that of azithromycin. It may be observed from this study that scaling and root planing + metronidazole + amoxicillin was the only treatment that significantly reduced the proportions of the three pathogens of the red complex. Moreover, the use of MET + AMOX as an adjunct to SRP was able to increase the proportions of three beneficial bacterial species (Actinomyces gerencseriae, A. naeslundii and Streptococcus sanguinis) as opposed to only one in the azithromycin group (A. naeslundii). All three treatments resulted in a beneficial change in the microbial profile; however, one important aspect to point out in this figure is the residual mean proportion of red complex in the three groups. These species accounted for approximately 12% of the 40 species evaluated in the scaling and root planing and azithromycin groups, and for 4.9% in the metronidazole + amoxicillin group. Previous publications have demonstrated a mean of 10% remaining red complex in subjects with advanced periodontitis treated by scaling and root planing (Silva et al, 2011). Therefore, 12% remaining mean proportions of red complex in the azithromycin-treated subjects was a rather disappointing result and is probably one of the major reasons for the lack of an additional clinical effect of azithromycin Table 2: Changes in probing depth and clinical attachment between baseline and 3 months, baseline and 6 months and baseline and 1 year post-treatment in 45 subjects with very advanced periodontitis treated with scaling and root planing alone, scaling and root planing combined with azithromycin, or scaling and root planing combined with metronidazole + amoxicillin. Adapted from Feres et al (2015) Baseline probing depth 10 Variables Time period Treatment groups P* 4 6 mm Probing depth reduction (mm) 7 mm Clinical attachment gain (mm) Probing depth reduction (mm) Clinical attachment gain (mm) SRP (n = 15) SRP + AZM (n = 15) SRP + MET + AMOX (n = 15) 0 3 months 1.3 ` 0.5 A 1.7 ` ` 0.5 B months 1.5 ` 0.4 A 1.6 ` ` 0.5 B year 1.5 ` 0.5 A 1.5 ` 0.4 A 2.1 ` 0.4 B months 0.9 ` 0.3 A 1.2 ` ` 0.5 B months 1.0 ` 0.3 A 1.2 ` ` 0.4 B year 1.1 ` 0.6 A 1.1 ` 0.4 A 1.8 ` 0.5 B months 2.5 ` 0.7 A 3.4 ` 0.6 B 3.9 ` 0.7 B months 2.8 ` 0.8 A 3.4 ` ` 0.8 B year 2.9 ` 0.8 A 3.3 ` ` 0.7 B months 1.5 ` 0.7 A 2.5 ` 0.6 C 3.0 ` 0.5 B months 1.8 ` 0.6 A 2.5 ` 0.6 C 3.4 ` 0.7 B year 2.0 ` 1.2 A 2.6 ` ` 0.6 B Values are given as mean ` SD. *The significance of differences among groups at each time point was assessed using one-way analysis of variance and Tukey s multiple comparison tests (different letters indicate significant differences between pairs of groups).

13 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited over that obtained with scaling and root planing only. These results indicate that azithromycin does not yield the same benefits of metronidazole + amoxicillin in the treatment of advanced chronic periodontitis (Feres, 2015). A more recent study evaluating the effect of adjunctive administration of azithromycin after non-surgical periodontal therapy showed that both azithromycin and placebo groups demonstrated similar improvements in all clinical parameters as well as MMP-8 levels in GCF (Han et al., 2012). This finding was supported by another publication from the same group, once again showing similar outcomes in MMP-8 levels and bacterial counts between patients treated with adjunctive azithromycin or placebo. However, in this study, a significant improvement in terms of pocket depth and number of deep sites was noted in the azithromycin group at one month (Emingil et al., 2012). Dastoor et al (2007) conducted a different double blind randomized placebo controlled study on smokers, which focused on clinical improvement following pocket elimination surgery (apically repositioned flap with osseous recontouring). The data presented suggested that surgical treatment of moderate and deep periodontal pockets in heavy smokers improved CAL gain and PD reduction as well as BOP. However, the adjunctive administration of systemic azithromycin to surgical treatment did not improve overall PD reduction or CAL gain, compared to sites that received surgical treatment only. For teeth that were treated nonsurgically, the systemic administration of azithromycin furthermore yielded significant gains in overall CAL compared to baseline, whereas placebo did not. Although it would require more research to confirm these results, the authors also found that the addition of AZM during periodontal surgery in heavy smokers promoted rapid wound healing, as well as reduced short term gingival inflammation as measured according to a wound healing index. It was also found that azithromycin resulted in less plaque formation within 3 months although no explanation for this could be presented (Dastoor et al., 2007). In order to negate the limitations in study design, a further study by Yashima et al (2009), was conducted by the same group to evaluate the effect staged mechanical debridement had if performed during the effective half life of azithromycin, compared to full mouth debridement. It was once again found that both staged SRP and full mouth debridement led to statistically significant improvements in terms of AL and PD as well as improvements in the microbiological profile compared to baseline values. However, there was no significant difference between the test and control group Local Azithromycin Local applications of azithromycin have also been studied (Pradeep et al., 2008). In this study eighty patients were either treated with SRD only or with SRD with adjunct azithromycin which was prepared as a PLGA in situ gel at a concentration of 0.5% and placed into the gingival sulcus after debridement. For both clinical parameters (CAL and PD) there was a significant improvement from baseline, as well as a significant difference between groups at 3 months. In terms of microbiological parameters used, there was also a significant improvement from baseline and between the groups (Pradeep et al., 2008). However, in this study, the differences in reductions in PD (0.4 mm) and CAL (0.6 mm) at the 3 month time point are so small that one could question the clinical relevance. Furthermore the trial was neither placebo controlled nor blinded which leaves results at risk for bias. Azithromycin in other periodontal diseases When evaluated for its efficacy to reduce bacterial numbers in periodontal abscesses without mechanical debridement, it was found that azithromycin was equally as effective as augmentin 500 mg in reducing the numbers of several periodontal pathogens such as P. gingivalis, P. intermedia, B. forsythus, P. micros and F. nucleatum (Herrera et al., 2000). Studies have suggested that azithromycin may have the potential to exert anti-inflammatory and healing properties. The resolution of cyclosporine-induced gingival overgrowth over time is a pointer to the drugs long-term host-modulatory/ healing properties. The property of azithromycin to reduce drug-related gingival overgrowth is generally unknown in the periodontal literature as it has not translated to clinical practice, texts or significant periodontal research. Azithromycin and Peri-implantitis Peri-implantitis (PI) is an inflammatory condition characterized by loss of supporting bone in the tissues surrounding the implant. Clinical signs of PI include gingival bleeding, suppuration, increased pocket depth, alveolar bone loss and implant mobility. Bacterial colonization on oral implant surfaces occurs rapidly. Pseudomonas aeruginosa, a key pathogen in quorum sensing in biofilm structures also appears to attach easily to titanium surfaces (Peltonen et 11

14 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited al. 2007). Pseudomonas aeruginosa and Staphylococcus aureus have both been identified in oral titanium related peri-implant lesions (Persson et al. 2011). In addition, studies have also shown a similarity in bacterial flora associated with PI and periodontitis. Various treatment regimes for PI have been proposed in the literature. These include plaque control regimens, mechanical debridement of the affected areas, irrigation with antiseptic agents [such as chlorhexidine (CHX), saline and 10% hydrogen per oxide], surgical flap access into infected peri-implant tissues and laser therapy. It is suggested that local or systemic delivery of antibiotics with traditional PI treatment regimes eliminates periodontol pathogenic bacteria to a greater extent compared with when these treatment regimes are performed alone. This may in turn facilitate healing of PI sites. However, there is no scientific evidence that could support this approach and none of the reports available have used a control group. Thus the clinical efficacy of antibiotics as adjuncts to conventional PI therapy is rather dubious. There is an urgent need for double-blinded placebo-controlled randomized clinical trials to demonstrate the efficacy of locally delivered and systemically delivered antibiotics in the treatment of PI (Javed et al, 2013). Probably, the only randomized control trial available is the study by Hallstrom et al (2012). The authors evaluated the added benefit of adjunct azithromycin to non surgical debridement for the treatment of peri-implant mucositis. In total 48 patients were treated either with debridement alone or with debridement and azithromycin and it was found that there was no added benefit of the adjunct use of the antimicrobial. However, this should be seen in the context of the known efficacy of mechanical therapy alone in the treatment of perimucositis, which may be sufficient to resolve local inflammation (Heitz-Mayfield et al., 2011, Renvert et al., 2008). Conclusion In conclusion, we could say that the use of azithromycin as an adjunct to periodontal therapy has demonstrated in general to provide clinical benefits over SRP alone, particularly at initially deeper periodontal pockets or periodontaly affected smokers. On the other hand, many of the subjects showed a good clinical response after SRP only. Therefore, we could say that the use adjunctive antibiotics should reserved for subjects with moderate to advanced periodontal disease in whom such agents would provide the maximum benefit. This article also highlighted that there is not current agreement of the literature and that not all studies have responded clinically in the same fashion, indicating the importance of determining factors that impact treatment outcome so that the most appropriate therapy can be provided to individual subjects. At this point, when we compared azithromycin with Amoxicillin + Metronidazole, azithromycin does not seem to be better for the treatment of periodontal infections. This might be related to the fact that azithromycin is a bacteriostatic drug, as opposed to metronidazole and amoxicillin, which are bactericidal. However, the short dosage therapy, minimum side effects and the promising role of azithromycin as a host modulation drug, makes this antibiotic a valuable drug to take into account in future research and as adjunct to periodontal therapy. References Albandar, J. M. & Tinoco, E. M. (2002) Global epidemiology of periodontal diseases in children and young persons. Periodontol , Altenburg J, de Graaff CS, van der Werf TS, Boersma WG. (2011) Immunomodulatory effects of macrolide antibiotics part 1: biological mechanisms. Respiration 81, Axelsson P, Lindhe J. (1981) The significance of maintenance care in the treatment of periodontal disease. J Clin Periodontol 8, Buchter A, Meyer U, Kruse-Losler B et al. (2004) Sustained release of doxycycline for the treatment of peri-implantitis: randomised controlled trial. Br J Oral Maxillofac Surg 42, Dastoor SF, Travan S, Neiva RF, Rayburn LA, Giannobile WV, Wang HL. (2007) Effect of adjunctive systemic azithromycin with periodontal surgery in the treatment of chronic periodontitis in smokers: a pilot study. J Periodontol 78, Emingil G, Han B, Ozdemir G, Tervahartiala T, Vural C, Atilla G, Baylas H, Sorsa T. (2012) Effect of azithromycin, as an adjunct to nonsurgical periodontal treatment, on microbiological parameters and gingival crevicular fluid biomarkers in generalized aggressive periodontitis. J Perio Res 47, Feres M, Soares GMS, Mendes JAV, Silva MP, Faveri M, Teles R, Socransky SS, Figueiredo LC. (2012) Metronidazole alone or with amoxicillin as adjuncts to nonsurgical treatment of 12

15 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited chronic periodontitis: a 1-year double-blinded, placebocontrolled, randomized clinical trial. J Clin Periodontol: 39, Gladue RP, Bright GM, Isaacson RE, Newborg MF. (1989) In vitro and in vivo uptake of azithromycin by phagocytic cells: possible mechanism of delivery and release at sites of infection. Antimicrob Agents Chemother 33, Gladue RP, Snider ME. (1990) Intracellular accumulation of azithromycin by cultured human fibroblasts. Antimicrob Agents Chemother 34, Gomi K, Yashima A, Nagano T, Kanazashi M, Maeda N, Arai T. (2007) Effects of full-mouth scaling and root planing in conjunction with systemically administered azithromycin. J Periodontol 78, Guerrero, A., Griffiths, G. S., Nibali, L., Suvan, J., Moles, D. R., Laurell, L. & Tonetti, M. S. (2005) Adjunctive benefits of systemic amoxicillin and metronidazole in nonsurgical treatment of generalized aggressive periodontitis: a randomized placebo-controlled clinical trial. J Clin Periodontol 32, Haas AN, de Castro GD, Moreno T, Susin C, Albandar JM, Oppermann RV, Rosing CK. (2008) Azithromycin as an adjunctive treatment of aggressive periodontitis: 12-months randomized clinical trial. J Clin Periodontol 35, Haas AN, Silva-Boghossian CM, Colombo AP, Susin C, Albandar JM, Oppermann RV, Rosing CK. (2012) Adjunctive azithromycin in the treatment of aggressive periodontitis: microbiological findings of a 12-month randomized clinical trial. J Dent 40, Haas AN, de Castro GD, Moreno T, Susin C, Albandar JM, Oppermann RV, Ro sing CK. (2008) Azithromycin as an adjunctive treatment of aggressive periodontitis: 12-months random- ized clinical trial. J Clin Periodontol 35, Haffajee AD, Socransky SS, Gunsolley JC. Systemic antiinfective periodontal therapy. A systematic review. (2003) Ann Periodontol 8, Haffajee AD, Torresyap G, Socransky SS. (2007) Clinical changes following four different periodontal therapies for the treatment of chronic periodontitis: 1-year results. J Clin Periodontol 34, Haffajee AD, Socransky SS, Patel MR, Song X. (2008) Microbial complexes in supragingival plaque. Oral Microbiol Immunol 23, Hallstrom H, Persson GR, Lindgren S, Olofsson M, Renvert S. (2012) Systemic antibiotics and debridement of peri-implant mucositis. A randomized clinical trial. J Clin Periodontol 39, Han B, Emingil G, Ozdemir G, Tervahartiala T, Vural C, Atilla G, Baylas H, Sorsa T. (2012) Azithromycin as an adjunctive treatment of generalized severe chronic periodontitis: clinical, microbiological and biochemical parameters. J Periodontol 83, Heitz-Mayfield, LJA (2009) Systemic antibiotics in periodontal therapy. Aust Dent J 54:(1 Suppl), S96 S101 Heitz-Mayfield LJ, Salvi GE, Mombelli A et al. (2012) Antiinfective surgical therapy of peri-implantitis. A 12-month prospective clinical study. Clin Oral Implants Res 23, Henry DC, Riffer E, Sokol WN, Chaudry NI, Swanson RN. (2003) Randomized double-blind study comparing 3- and 6-day regimens of azithromycin with a 10-day amoxicillinclavulanate regimen for treatment of acute bacterial sinusitis. Antimicrob Agents Chemother 47, Herrera, D., Roldan, S., O Connor, A. & Sanz, M. (2000a) The periodontal abscess (II). Short term clinical and microbiological efficacy of 2 systemic antibiotic regimes. J Clin Periodont 27, Herrera, D., Sanz, M., Jepsen, S., Needleman, I. & Roldan, S. (2002) A systematic review on the effect of systemic antimicrobials as an adjunct to scaling and root planing in periodontitis patients. J Clin Periodont 29 (Suppl. 3), ; discussion Hirsch R, Deng H, Laohachai MN. (2012) Azithromycin in periodontal treatment: more than an antibiotic. J Periodont Res 47, Hoepelman IM, Schneider MME. (1995) Azithromycin: the first of the tissue-selective azalides. Int J Antimicrob Agents 5, Javed F, AlGhamdi AST, Ahmed A, Mikami T, Ahmed HB, Tenenbaum HC (2013) Clinical efficacy of antibiotics in the treatment of peri-implantitis. Int Dent J 63, Kornman KS. (2008) Mapping the pathogenesis of periodontitis: A new look. J Periodontol 79(Suppl. 8), Kornman KS, Page RC, Tonetti MS. (1997) The host response to the microbial challenge in periodontitis: Assembling the players. Periodontol ,

16 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited Lavanchy DL, Bickel M, Baehni PC. (1987) The effect of plaque control after scaling and root planing on the subgingival microflora in human periodontitis. J Clin Periodontol 14, Lai PC, Ho W, Jain N, Walters JD. (2011) Azithromycin concentrations in blood and gingival crevicular fluid after systemic administration. J Periodontol 82, Leonhardt A, Dahlen G, Renvert S. (2003) Five-year clinical, microbiological, and radiological outcome following treatment of peri-implantitis in man. J Periodontol 74, McDonald PJ, Pruul H. (1991) Phagocyte uptake and transport of azithromycin. Eur J Clin Microbiol Infect Dis 10, Marsh PD. (2005) Dental plaque: biological significance of a biofilm and community lifestyle. J Clin Periodontol 32 (Suppl 6), Mascarenhas P, Gapski R, Al-Shammari K, Hill R, Soehren S, Fenno JC, Giannobile WV, Wang HL. (2005) Clinical response of azithromycin as an adjunct to non-surgical periodontal therapy in smokers. J Periodontol 76, Mombelli A, Lang NP. (1992) Antimicrobial treatment of peri-implant infections. Clin Oral Implants Res 3, Oteo A, Herrera D, Figuero E, O Connor A, Gonzalez I, Sanz M. (2010) Azithromycin as an adjunct to scaling and root planing in the treatment of Porphyromonas gingivalisassociated periodontitis: a pilot study. J Clin Periodontol 37, Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman KS. (1997) Advances in the pathogenesis of periodontitis: Summary of developments, clinical implications and future directions. Periodontol , Pajukanta, R. (1993) In vitro antimicrobial susceptibility of Porphyromonas gingivalis to azithromycin, a novel macrolide. Oral Microbiol and Immunology 8, Palmer, R. M., Watts, T. L. P. & Wilson, R. F. (1996) A double-blind trial of tetracycline in the management of early onset periodontitis. J Clin Periodont 23, Pavicic MJ, van Winkelhoff AJ, de Graaff J. (1992) In vitro susceptibilities of Actinobacillus actinomycetemcomitans to a number of antimicrobial combinations. Antimicrob Agents Chemother 36, Pradeep AR, Sagar SV, Daisy H. (2008) Clinical and microbiologic effects of subgingivally delivered 0.5% azithromycin in the treatment of chronic periodontitis. J Periodontol 79, Pradeep AR, Bajaj P, Agarwal E et al. (2013) Local drug delivery of 0.5% azithromycin in the treatment of chronic periodontitis among smokers. Aust Dent J 58, Ray WA, Murray KT, Hall K, Arbogast PG, Stein CM. (2012) Azithromycin and the risk of cardiovascular death. N Engl J Med 366, Renvert S, Lessem J, Dahlen G et al. (2008) Mechanical and repeated antimicrobial therapy using a local drug delivery system in the treatment of peri-implantitis: a randomized clinical trial. J Periodontol 79, Retsema, J., Girard, A., Schelkly, W., Manousos, M., Anderson, M., Bright, G., Borovoy, R., Brennan, L. & Mason, R. (1987) Spectrum and mode of action of azithromycin (CP- 62,993), a new 15-membered-ring macrolide with improved potency against gram- negative organisms. Antimicrobial Agents and Chemotherapy 31, Salvi GE, Persson GR, Heitz-Mayfield LJ et al. (2007) Adjunctive local antibiotic therapy in the treatment of periimplantitis II: clinical and radiographic outcomes. Clin Oral Implants Res 18, Sampaio E, Rocha M, Figueiredo LC, Faveri M, Duarte PM, Gomes Lira EA, Feres M. (2011) Clinical and microbiological effects of azithromycin in the treatment of generalized chronic periodontitis: a randomized placebo-controlled clinical trial. J Clin Periodontol 38, Saxen L, Asikainen S. (1993) Metronidazole in the treatment of localized juvenile periodontitis. J Clin Periodont 20, Sbordone L, Ramaglia L, Gulletta E, et al. (1990) Recolonization of the subgingival microflora after scaling and root planing in human periodontitis. J Periodontol 61, Schentag JJ, Ballow CH. (1991) Tissue-directed pharmacokinetics. Am J Med 91, 5S 11S. Sefton, A. M., Maskell, J. P., Beighton, D., Whiley, A., Shain, H., Foyle, D., Smith, S. R., Smales, F. C. & Williams, J. D. (1996) Azithromycin in the treatment of periodontal disease. Effect on microbial flora. J Clin Periodont 23, Smith SR, Foyle DM, Daniels J, Joyston-Bechal S, Smales FC, Sefton A, Williams J. A. (2002) Double-blind placebo controlled trial of azithromycin as an adjunct to nonsurgical treatment of periodontitis in adults: clinical results. J Clin Periodontol 29,

17 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited Silva MP, Feres M, Sirotto TA, Soares GM, Mendes JA, Faveri M, Figueiredo LC. (2011) Clinical and microbiological benefits of metronidazole alone or with amoxicillin as adjuncts in the treatment of chronic periodontitis: a randomized placebo-controlled clinical trial. J Clin Periodontol 38, Sgolastra F, Severino M, Petrucci A, Gatto R, Monaco A. (2014) Effectiveness of metronidazole as an adjunct to scaling and root planing in the treatment of chronic periodontitis: a systematic review and meta-analysis. J Periodontal Res 49, Slots J, Mashimo P, Levine MJ, Genco RJ. (1979) Periodontal therapy in humans. I. Microbiological and clinical effects of a single course of periodontal scaling and root planing, and of adjunctive tetracycline therapy. J Periodontol 50, Tinoco, E. M., Beldi, M. I., Campedelli, F., Lana, M., Loureiro, C. A., Bellini, H. T., Rams, T. E., Tinoco, N. M., Gjermo, P. & Preus, H. R. (1998) Clinical and microbiological effects of adjunctive antibiotics in treatment of localized juvenile periodontitis. A controlled clinical trial. J Periodontol 69, van Winkelhoff, A. J., Herrera Gonzales, D., Winkel, E. G., Dellemijn-Kippuw, N., Van- denbroucke-grauls, C. M. & Sanz, M. (2000) Antimicrobial resistance in the subgingival microflora in patients with adult periodontitis. A comparison between The Netherlands and Spain. J Clin Periodont 27, Yashima A, Gomi k, Maeda N, Arai T. (2009) One-stage full-mouth versus partial-mouth scaling and root planing during the effective half-life of systemically administered azithromycin. J Periodontol 80, NEW SOUTH WALES BRANCH AUSTRALIAN SOCIETY OF PERIODONTOLOGY NEW SOUTH WALES BRANCH Presents: 2017 SPONSORS Professor Marco Esposito FULL DAY SEMINAR Implant dentistry, an evidence-based overview Friday, 3 November 2017 Doltone House - Hyde Park Prof Marco Esposito Details and registration form: Enquiries: helen.mooney4@gmail.com Early bird registration closes Friday, 6 October ASP NSW guarantee their courses are compliant with Section 4 of the DBA Guidelines on Continuing Professional Development 15

18 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited Colonisation of the Oral Cavity: Birth to Late Teenage Years Fiona K. Chan Introduction The oral cavity harbours a diverse microbiome which exists as structurally-organised biofilms on mucosal and dental surfaces (Marsh et al., 2015). As a child matures and develops from birth, the complexity of this microbiota increases and evolves. The host immune response, microbial virulence factors and environmental changes can influence the colonization of the oral cavity and composition of the biofilm. Whilst the indigenous microbiota plays an important role in the protection of the host, a disruption in the balance of the microbial ecosystem can result in disease. Numerous studies comparing the microbiota from healthy and diseased sites have demonstrated that there are substantial differences in the composition of the biofilm (Chen & Jiang, 2014; Socransky et al., 1998; Wade, 2013). Therefore, a thorough understanding of the acquisition and colonisation of microbial species from infancy to late teenage years is crucial to better understanding disease initiation. This review article will present an overview of the current literature describing the colonisation of the oral cavity form birth to late teenage years. Development of the oral biofilm The oral cavity harbours a diverse microbiome which includes viruses, fungi, protozoa, archaea and bacteria (Wade, 2013). However, bacteria are the most common and numerous within the human mouth. The formation of the oral biofilm involves the ordered colonization by a range of bacteria and this can form on the hard and soft structures in the oral cavity (Marsh, 2000). In the developing biofilm, initially there is formation of a conditioning film composed of salivary glycoproteins which enhances bacterial adhesion (Walsh, 2009). This is followed by the seeding of primary bacterial colonisers in the acquired pellicle. Secondary bacterial colonisers then attach to the primary colonisers which join the developing biofilm via co-aggregation interactions. The sequential colonisation by other organisms and multiplication of the bacteria lead to Abstract: The oral cavity harbours a diverse microbiome which exists as structurally-organised biofilms on mucosal and dental surfaces (Marsh, Head, & Devine, 2015). As a child matures and develops from birth to adolescence, the complexity of this microbiota increases and evolves. Whilst the indigenous microbiota plays an important role in the protection of the host, a disruption in the balance of the microbial ecosystem can result in disease. Therefore, a thorough understanding of the acquisition and colonisation of microbial species from infancy to late teenage years is crucial to better understanding disease initiation. Aim: This review article will present an overview of the current literature describing the colonisation of the oral cavity form birth to late teenage years. Materials and methods: A PubMed search was conducted and the literature was reviewed. A hand search of references in key review papers was also performed. Results and conclusion: Dental disease results from an ecologic shift in the biofilm which may result in indigenous colonizers becoming opportunistic pathogens. A consortium of bacteria has been associated with periodontal disease and the red complex has been implicated as one of the major causative agents. Whilst identification of potential causative agents of periodontal disease allows for a greater understanding of the overall disease process, as yet, no single cause of periodontal infections has been identified. Therefore, the clinician s treatment should be guided by the nature of the infecting microorganisms and the host response. Further research is required to enhance our understanding of the colonisation of the oral cavity from infancy to late teenage years. Keywords: oral colonisation, infancy, teenage, aggressive periodontitis 16

19 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited an increase in the biomass. The outcome of this microbial succession leads to an increase in the complexity and thickness of the biofilm over time. Finally, an equilibrium state or climax community is reached where there is a balance between biofilm growth and loss of bacteria into the environment (Marsh & Bradshaw, 1995). As the biofilm develops, symbiotic and amphibiotic relationships form between species to confer metabolic advantages (Ruby & Goldner, 2007). The ecological plaque hypothesis forms the basis of the contemporary understanding of the dental disease process. It hypothesizes that the oral ecology as a whole contributes to the aetiology of plaque-related diseases. The stable oral biofilm can become pathogenic if environmental perturbations triggers a catastrophic shift in the balance of the resident microflora (Marsh & Bradshaw, 1995). In 1998, Socransky et al. proposed that the microflora in plaque could be better understood by focusing on the consortia of organisms that successively colonise the oral cavity. Five sets of bacterial complexes were identified and initial colonisation involved members of the yellow, green and purple complexes along with the Actinomyces species. These initial colonizers conditioned the subsequent colonisation and autogenic succession of more organisms. The more periopathogenic bacteria (i.e. red complex) depended on the earlier colonization of the relatively less pathogenic organisms (i.e. orange complex). It was hypothesized that the dominance of the red and orange complexes could lead to a shift in the climax community resulting in disease progression (Socransky et al., 1998). Influences on colonisation of the oral cavity Host response The host immune system can influence the colonising ability of microbes in the oral cavity. Infants are particularly susceptible to microbial colonization as their immune systems are immature and specific antibodies, such as secretory immunoglobulin A (S-IgA), are present at relatively low levels at this time (Könönen, 2000). S-IgA constitutes one of the main defence mechanisms on oral mucosal surfaces as it can inhibit microbial adherence (Williams & Gibbons, 1972). In infants, the ability of the host to defend against pathogens is further hampered by the ability of some early colonizing bacteria to specifically cleave IgA1 in vivo (Frandsen et al., 1995; Kilian et al., 1996). Whilst the saliva also contains a number of innate non-immunoglobulin defence factors, the naivety of the immune system renders the microbial colonisation in the oral cavity of an infant relatively easy. Circumstances for bacterial colonisation Adhesion is the initial step in bacterial colonisation and it is crucial for bacterial attachment and growth. In edentulous infants, the epithelial surfaces provide a niche environment for bacterial adhesion and colonization. With the eruption of teeth, however, a greater surface area for adherence and retention of microbes results in an increase in the number and diversity of the bacterial microbiome. The rate and extent of colonization in the oral cavity of a neonate also depends on various factors, such as the gestational age, exposure to antibiotic treatment, hospitalization in an intensive care unit, type and mode of feeding (Makhoul et al., 2002). This variability is highlighted in the distinct differences in the early microflora of preterm neonates requiring prolonged hospital care and normal neonates (Rotimi & Duerden, 1981). Whilst it is clear that the composition of the oral flora can be influenced by changes in the environment, host genetics has also been proposed as an influencing factor on bacterial colonization. Moore et al. examined twin children living in the same households and found that the subgingival microflora of identical twins were more similar than those of fraternal twins, indicating that there may be some genetic control over the composition of the microflora (Moore et al., 1993). Bacterial virulence factors Virulence factors can influence the ability of bacteria to adhere to different surfaces in the oral cavity. Fimbriae have been detected on A. naeslundii (Handley et al., 1985), P. gingivalis (Yoshimura, 1984), A. actinomycetemcomitans (Rosan et al., 1988) and some strains of streptococci such as S. salivarius (Handley, Carter, & Fielding, 1984) and have been proposed as important mechanisms in the adherence to oral surfaces. Factors that promote A. actinomycetemcomitans colonization and its persistence in the oral cavity include adhesins, bacteriocins, invasins and an ability to elicit its own uptake into epithelial cells and spread to adjacent cells by usurping normal epithelial cell function (Fives-Taylor et al., 1999). However, successful colonisation of the oral cavity is also dependent on basic bacterial growth and survival requirements being met. These include the ability to adhere to appropriate surfaces, presence at a colonisable place at the correct time, possession of a survival capability 17

20 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited permitting prolonged viability in deleterious circumstances, ability to obtain all nutrients from the ecosystem, possession of mechanisms to overcome or cope with environmental resistance attributable to viable hosts and species already in the habitat and a capacity to tolerate all the ecologically significant non-microbial factors of the environment (e.g. temperature, osmotic pressure, oxidation-reduction potential, ph, O2 levels) (Socransky & Haffajee, 2005). Transmission of oral pathogens At birth, the oral cavity is usually void of microbes. However, oral microbes start to colonize an infant s mouth soon after birth as they are exposed to microbial sources from the external environment (Könönen et al., 1994; Pearce et al., 1995; Rotimi & Duerden, 1981). Potential sources for the developing oral microflora in infants include pacifiers, breast feeding or bottle feeding. However, saliva from the mother appears to be the main vehicle for bacterial transmission to the infant. Vertical transmission from mother to child is believed to be the major route of oral bacteria acquisition (Berkowitz & Jordan, 1975; Könönen, Asikainen, & Jousimies-Somer, 1992; Masuda et al., 1985). A high degree of homology between S. mutans strains recovered among members of the same family has been demonstrated, indicating both vertical and horizontal routes of transmission (Köhler et al., 2003). Moreover, transmission of C. albicans vertically from mother to infant and nosocomical transmission of both albicans and non-albicans species of Candida has also been documented (Pfaller et al., 1998; Waggoner-Fountain et al., 1996). Periodontopathogenic bacteria are transmissible among family members and numerous studies have suggested that children acquire the pathogens predominantly from their parents (Alaluusua et al., 1993; Könönen, Jousimies- Somer, & Asikainen, 1992). Identical ribotypes of P. melaninogenica has been demonstrated in six of eleven mother-child pairs and it has been proposed that the most likely mode of transmission of this periodontal organism is through saliva (Könönen et al., 1994). Könönen et al. also demonstrated that when maternal salivary levels of P. melaninogenica, F. nucleatum non-pigmented Prevotella spp., P. intermedia and P. loescheii exceeded 104 CPU/mL, the infants colonisation frequency of P. melaninogenica and F. nucleatum doubled (Könönen et al., 1992). In addition, the intrafamilial transmission of A. actinomycetemcomitans has been demonstrated, with seven out of nine families sharing an identical ribotype of A. actinomycetemcomitans (Alaluusua et al., 1993). This observation has been further supported by studies which demonstrated identical A. actinomycetemcomitans genotypes isolated from members of the same family (Asikainen, Chen, & Slots, 1996; Christersson, 1993; Zambon, Christersson, & Slots, 1983). Colonisation of the oral cavity in the infant The colonisation of the oral cavity is influenced by host, microbial and environmental factors. Whilst it is recognised that the biofilm is dynamic and the microbial profile can vary considerably between individuals, numerous studies have attempted to examine the composition of the oral microbiota at different stages of development. At birth the oral cavity is essentially sterile; however, within hours after delivery, the infant s oral cavity becomes colonized by low numbers of mainly facultative and aerobic bacteria (Socransky & Manganiello, 1971). As infants have no teeth, the epithelial surfaces in the oral cavity of newborns provide niches for bacterial colonization. Whilst there is great variability in the bacterial composition of the oral cavity in the first few days of life, organisms that are able to adhere to the mucous membranes can become well established in the oral cavity. Early colonisers include the Streptococci genus which possesses the ability to coaggregate bacteria of the same genus as well as species of other genera (Kolenbrander, 2000; Kolenbrander, Andersen, & Moore, 1990). S. salivarius, S. mitis and S. oralis have been identified as the predominant pioneer oral microbes to colonize the oral cavities of newborn infants (Law, Seow, & Townsend, 2007; Smith et al., 1993). Furthermore, Streptococci have been reported to comprise 98% of the cultivable bacteria within 2 days of birth and 70% after 12 months (Cortelli et al., 2008; McCarthy, Snyder, & Parker, 1965). Neisseria spp., Actinomyces spp. and Staphylococcus spp. have also been identified as primary colonizers of the oral cavity (Newman et al., 2012). The initial colonization by Streptococci spp. and Actinomyces spp. conditions further colonization by other bacterial species through species-specific adhesion and receptor molecules (Kolenbrander & Andersen, 1986). As early as the second day of life, it is possible to detect some anaerobic species in an infant s edentulous mouth (Rotimi & Duerden, 1981). Six different gram negative anaerobic bacterial species (P. melaninogenica, F. nucleatum, Veillonella spp., non-pigmented Prevotella spp., Bacteroides gracilis, Capnocytophaga spp.) have been detected in infants up to 1 month of age and three additional species 18

21 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited (P. loescheii, P. intermedia, E. corrodens) up to 2 months of age (Frisken, Higgins, & Palmer, 1990; Könönen et al., 1992). Similarly, a longitudinal study by Könönen et al. has demonstrated that the obligately anaerobic Veillonella spp. and P. melaninogenica are early colonizers, becoming established within the first 2 months of life (Könönen et al., 1999). F. nucleatum, non-pigmented Prevotella spp., Leptotrichia spp. and P. catoniae have been occasionally retrieved from subjects at two months of age but are frequent findings by the time the infant is one years old (Könönen et al., 1999). F. nucleatum has been found to be the most frequent strictly anaerobic species in infants during their first year of life and was detected in the oral cavity even before the eruption of teeth (Könönen et al., 1992). Species in the Fusobacterium genus act as bridging species between early and late colonizers (Kolenbrander, 2000; Kolenbrander et al., 1990; Kolenbrander & London, 1993; Whittaker & Klier, 1996). In addition, the presence of F. nucleatum in mixed cultures has been shown to be essential for other anaerobic species to survive under aerated conditions, which suggests that F. nucleatum is a key species in intergeneric bacterial coaggregation and biofilm formation (Bradshaw et al., 1998). Among the late colonizers, the prevalence of Capnocytophaga spp. increased to 10% towards the end of the first year of life (Könönen et al., 1999). Oral carriage of candida species has also been described as one of the most frequent yeast involved colonization of the oral cavity, with C. albicans being the most frequently isolated species in infants (Batista et al., 2014; Kleinegger et al., 1996). Oral carriage of candidal species in infants ranges from 8% to 77% (Ashbee & Bignell, 2009; Rozkiewicz et al., 2006; Sánchez-Vargas et al., 2005). Colonisation of the oral cavity in the mixed dentition stage Numerous studies have demonstrated that the complexity of the microflora in the oral environment increases with the eruption of teeth (Carlsson, Grahnén, & Jonsson, 1975; Pearce et al., 1995; Rotimi & Duerden, 1981). After the first year of life, remarkable increases in the frequency of several oral anaerobic groups occur (Könönen et al., 1999). Early colonizing species can be isolated from nearly every mouth and late colonizers such as Capnocytophaga spp., Selenomonas spp., and the P. intermedia (including P. nigrescens and P. pallens) are frequently detected in the oral cavity before four years of age (Könönen et al., 1994). It has been proposed that increased bacterial colonization occurs as the eruption of teeth offer a greater number of suitable niches and attachment sites for growth; however, it should also be noted that the more mature biofilms on oral surfaces also offer a more favourable microenvironment for the colonisation of anaerobes (Costerton et al., 1994). During the first three years of life, A. actinomycetemcomitans, P. gingivalis and T. forsythia has reportedly been absent (Frisken et al., 1990; Könönen et al., 1999). This is in contrast to a study by Tanner et al. examining the microbiota of children aged 6-36 months (Tanner et al., 2002). Putative periodontal pathogens, such as A. actinomycetemcomitans, P. gingivalis and T. forsythia, have been detected even in the youngest children of the study (6-18 months); however, there was a tendency for higher detection in the older children (19-36 months). A similar trend was noted in a study by Papaioannou et al. which found that the levels of the red complex pathogens, P. gingivalis, T. forsythia and T. denticola, remained very low, with values around 1% of the total microbiota for all age groups and all habitats in the younger age group (Papaioannou et al., 2009). However, a shift towards the more pathogenic complexes in the subgingival region, especially in older children (9-12 years) was observed especially for P. gingivalis and T. denticola, although these differences did not reach significant levels. In the early mixed and mixed dentition stage, C. showae, a member of the orange complex, increased significantly with age both supragingivally and subgingivally. The detection levels of A. actinomycetemcomitans and P. gingivalis in the oral microbiota of healthy children vary considerably between studies. A. actinomycetemcomitans was detected in 13% of healthy Finnish children aged between 4 and 7 years with deciduous teeth (Alaluusua & Asikainen, 1988). On the other hand, Morinushi et al. reported that A. actinomycetemcomitans was present in 85% of samples and P. gingivalis was detected in the subgingival plaque of over 60% of the children aged between 2 and 18 years (Morinushi et al., 2000). It was concluded that the presence of these two pathogens were closely related to the onset and severtiy of gingivits in healthy children above the age of 3 years (Morinushi et al., 2000). Similary, Nakagawa et al investigated the prevalence A. actinomycetemcomitans in young patients with gingivitis and found that 20% of preschool age children (mean age 4.5 years) harboured his bacteria; however, only 10% of early school age children (mean age 9.1 years) harboured A. actinomycetemcomitans in their plaque samples (Nakagawa et al., 1994). A. 19

22 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited actinomycetemcomitans has been reported to be more prevalent between 10 and 19 years of age; however, there is a decreasing prevalence with older age groups (Savitt & Kent, 1991). P. gingivalis has been isolated from the oral cavities of young healthy children; however, like A. actinomycetemcomitans, the distribution and detection levels vary considerably between studies. In a recent study, it was reported that 68.8% of healthy children between 18 to 48 months of age harboured P. gingivalis (Yang et al., 2002). In a different population, 36% to 43% of children between 0 and 18 years of age harboured P. gingivalis (Lamell et al., 2000) which was similar to the detection rates of P. gingivalis from children in the USA which was recovered from approximately 40% of the study population (McClellan, Griffen, & Leys, 1996). Conversely, detection rates in a Finnish population between 11 and 20 years of age for P. gingivalis was only 5% (Matto et al., 1998). In a Japanese population with a mean age of 8.3 years, P. gingivalis was detected in 8.9% of the cohort which seems to correlate with the findings in the Finnish study (Umeda et al., 2004). A. naeslundii, a predominant species of dental plaque, was reported to be absent in edentulous infants but gradually increased in prevalence as the child matured, with half the children colonized by age seven (Ellen, 1976). Veillonella spp. also followed a similar pattern of increasing prevalence with increasing age (McCarthy et al., 1965). The colonization of S. mutans and S. sanguis in the oral cavity occurred as teeth erupted during the first year of life (Carlsson et al., 1975; Könönen, 2005). Berkowitz et al. reported that S. mutans was absent from ninety one pre-dentate infants but was detected in 22% children who only had primary incisor teeth (Berkowitz, Jordan, & White, 1975). These findings were similar to a longitudinal investigation by Carlsson et al. which reported that S. mutans was detected in 20% of infants between 12 months to 16 months of age (Carlsson et al., 1975). Whilst the stage of dental development was not mentioned in the study, the age range of 12 to 16 months is compatible with an infant having 6 to 10 primary teeth. It was also found that children harbouring both S. mutans and Lactobacilli spp. increased from 4% at 6 months to 13% at 12 and 18 months to 20% at 24 months, suggesting that the diversity of microbiota in the oral cavity increases as a child grows and matures (Plonka et al., 2012). The early colonisation of acquired strains of S. mutans has been found to persist into adulthood (Köhler et al., 2003). Colonisation of oral cavity in the permanent dentition In a longitudinal study by Moore et al. it was observed that the composition of the oral flora differed significantly at ages 11 and 14 in the same individual, indicating that a transition to the adult microbial composition may be initiated during puberty (Moore et al., 1993). Unpaired t-tests indicated that V. atypica, P. denticola, and P. melaninogenica were among the species that contributed most to changes in microbial composition during puberty (Moore et al., 1993). In a similar study looking at the differences in periodontal disease-associated microorganisms in subgingival plaque, Wojcicki et al. demonstrated that populations of black pigmented Bacteroides were very low in prepubescent children however they were much higher in circumpubertal and post-pubertal children. These findings supported the postulated relationship between hormone levels and black pigmented Bacteroides levels in subgingival plaque and suggested that the differences in the subgingival environment can profoundly influence the proportions of putative periodontopathic species in plaque (Wojcicki, Harper, & Robinson, 1987). In a study of a female population, the percentage of black pigmented Bacteroides was higher in subjects who were soon to experience menarche, as compared to the microflora recovered from circumpubertal and postpubertal females (Delaney, Ratzan, & Kornman, 1986). In 1988, Van Oosten et al published research demonstrating that black pigmented Bacteroides (B. intermedius and B. melaninogenicus) and spirochetes were frequently found in the subgingival microbiota of prepubertal children and this was correlated with the clinical signs of gingivitis (van Oosten et al., 1988). Likewise, in pre-pubertal children from Tanzania and the Netherlands, it was observed that small, medium size and large spirochetes were found in higher numbers in inflamed sites compared with non-inflamed sites (Mikx, Matee, & Schaeken, 1986). In a cohort aged between 11 and 14 years, very low levels of A. actinomycetemcomitans and P. gingivalis were reported at puberty; however, a relationship between the presence of puberty gingivitis and periodontal and microbiological conditions was demonstrated 6 years after puberty (Mombelli, Rutar, & Lang, 1995). Similarly, the presence of A. actinomycetemcomitans and P. gingivalis in the oral cavity has been closely related to the onset and severity of gingivitis in healthy children above the age of 3 years (Morinushi et al., 2000). 20

23 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited Aggressive Periodontitis A knowledge on the acquisition and carriage of potential periodontal pathogens and their connection with disease initiation is important as in many cases, the disease may have its onset in the primary or mixed dentition of children who are susceptible for the development of aggressive periodontitis (Könönen & Muller, 2014). Elevated proportions of A. actinomycetemcomitans and, in some populations, of P. gingivalis have been presented among secondary features of localised and generalised forms of aggressive periodontitis in the consensus report of the International Workshop on the Classification of Periodontal Diseases and Conditions (Lang et al., 1999). However, a review of the literature investigating localised and generalised aggressive periodontitis is complicated due to the varying criteria used to classify this disease entity in the past. For the purposes of this review, localised juvenile periodontitis and localised pre-pubertal periodontitis will be encompassed in the diagnosis of localised aggressive periodontitis. Whilst the term generalised aggressive periodontitis will include rapidly progressive periodontitis, generalized juvenile periodontitis, and post-juvenile periodontitis. A. actinomycetemcomitans has been associated with localized aggressive periodontitis (Slots, 1976). In 1983, Zambon et al. undertook a study to determine the prevalence of A. actinomycetemcomitans in periodontal pockets from a large subject group with localised juvenile periodontitis (Zambon et al., 1983). A. actinomycetemcomitans was detected in 28 out of 29 localised juvenile periodontitis patients. The presence of P. gingivalis has also been associated with localized aggressive periodontitis; however, not as strongly as A. actinomycetemcomitans (Albandar, Brown, & Löe, 1997; López, Mellado, & Leighton, 1996; Vandesteen et al., 1984) In a study of Chilean children, it was found that localized aggressive periodontitis was more frequently associated with P. gingivalis than P. intermedia (López et al., 1996). Capnocytophaga spp., E. corrodens, C. rectus, spirochetes and Eubacterium spp. have also been implicated in localised aggressive periodontitis (Han et al., 1991; Moore et al., 1982). In addition, co-infection with herpes simplex virus, human cytomegalovirus and Epstein-Barr virus-1 in deep sites of localised early-onset periodontitis has also been detected (Ting, Contreras, & Slots, 2000). Whilst initial studies implicated the dominance of A. actinomycetemcomitans in localised aggressive periodontitis, the current evidence indicates that the microbiology is multifactorial and P. gingivalis and P. intermedia may also be important causative agents (Darby & Curtis, 2001). Some studies have reported that in generalized aggressive periodontitis, the predominant subgingival organism is A. actinomycetemcomitans (Lopez, Mellado, & Leighton, 1996; Slots, Reynolds, & Genco, 1980; Zambon, 1985). Conversely, A. actinomycetemcomitans has not been detected, or detected only in a very small proportion, of generalised earlyonset periodontitis patients (Vandesteen et al., 1984; Williams et al., 1985). Specifically, the A. actinomycetemcomitans JP2 clone has been proposed to play an important role in the development of aggressive periodontitis in certain populations (Könönen & Muller, 2014). Haubek et al. conducted a population-based longitudinal study in young teenagers from Morocco and found that individuals who carried the JP2 clone of A. actinomycetemcomitans had a significantly increased risk of periodontal attachment loss (Haubek et al., 2008). A much less pronounced disease risk was found in those carrying non-jp2 clones only. It should be noted that the biofilm in generalized aggressive periodontitis also contains other bacterial species. P. gingivalis, P. intermedia and F. nucleatum have also been recovered from generalised aggressive periodontitis patients (Masunaga et al., 1990; Nishimura et al., 1990; Williams et al., 1985). Loesche et al. reported significantly higher proportions of P. gingivalis (as well as P. intermedia and P. melaninogenica) in generalized early-onset periodontitis subjects (Loesche et al., 1985). Conclusion A thorough knowledge of the species involved in the primary colonization of the oral cavity is important as the early colonisers form the basis for further colonisation. Whilst the initial colonisers can affect the composition of the developing oral microflora, it should be recognised that the colonisation of the oral cavity is also influenced by many other factors, including host immunity and environmental changes. Due to the paucity of longitudinal studies, there have been relatively few studies investigating the initial microbial colonization in the oral cavity of infants and children. As most of these cross-sectional studies offer a snapshot of the oral microbiome, it is unclear as to whether the detection of certain bacterial species indicates successful colonisation of the oral cavity or merely provides an indication of the transient presence of a pathogen. In addition, as there are technical difficulties in processing large numbers of samples and challenges in the collection of microbial samples from 21

24 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited an infant or child, there has been great variability in the collection and processing methods employed. In some studies, microbial samples were collected from the cheek or tongue with a swab, whilst others involved the collection of dental plaque. It should be noted, however, that bacterial profile differs markedly on the various intraoral surfaces (Tanner et al., 2002). As such, the microbiota collected from one location may not fully reflect the microbiota colonising the rest of the oral cavity. In addition, geographic and ethnic differences in the carriage of periodontopathogens should be considered when comparing studies in different study populations. Another limitation of some of the earlier studies was the use of culture based methods which relied heavily on the cultivability of microorganisms (Delaney et al., 1986; Frisken et al., 1990; Könönen et al., 1992; Moore et al., 1984). Due to the sophisticated methods needed for the culturing of anaerobic bacteria, some studies failed to detect obligate anaerobes in infants and young children in the earlier studies. This then led to the belief that colonization by anaerobic pathogens rarely takes place in early childhood. With the development of more sensitive techniques for detection, such as PCR-based methods, more accurate identification of microorganisms has been demonstrated. These newer techniques have enabled the characterisation of a wider diversity of bacterial species. Moreover, the detection of a greater number pathogens has been observed which, in some instances, can help to explain the significant variability among similar populations (Yang et al., 2002). However, even with the advent of these new technologies, many of the more recent studies have not explored the proportions and the prevalence of bacterial species within a sample population. In addition, little is known about the genetic influence on the colonization and composition of the oral microbiome. It is clear that further investigations including the use of prospective, longitudinal study designs are required to follow the changes from initial colonization to the progressing or active lesions. In summary, dental disease results from an ecologic shift in the biofilm which may result in indigenous colonizers becoming opportunistic pathogens. A consortium of bacteria has been associated with periodontal disease and the red complex has been implicated as one of the major causative agents. Whilst identification of potential causative agents of periodontal disease allows for a greater understanding of the overall disease process, as yet, no single cause has been identified. Therefore, the clinician s treatment should be guided by the nature of the infecting microorganisms and host response. Currently, there are no studies demonstrating that paediatric colonisation by putative periodontopathogens predisposes an individual to dental disease in adulthood. Nevertheless, knowledge of the changes in the microbiome that occur early in the development of periodontal disease could lead to more effective methods of preventing disease. Further research employing the latest microbiological techniques, may help to enhance our understanding of the colonisation of the oral cavity from infancy to late teenage years. Abbreviations A. actinomycetemcomitans = Aggregatibacter actinomycetemcomitans A. naeslundii = Actinomyces naeslundii B. gracilis = Bacteroides gracilis C. albicans = Candida albicans C. rectus = Campylobacter rectus C. showae = Campylobacter showae E. corrodens = Eikenella corrodens F. nucleatum = Fusobacterium nucleatum P. catoniae = Porphyromonas catoniae P. gingivalis = Porphyromonas gingivalis P. melaninogenica = Prevotella melaninogenica S. mitis = Streptococcus mitis S. oralis = Streptococcus oralis S. salivarius = Streptococcus salivarius T. denticola = Treponema denticola T. forsythia = Tanerella forsythia V. atypica = Veillonella atypica References Alaluusua, S., & Asikainen, S. (1988). Detection and distribution of Actinobacillus actinomycetemcomitans in the primary dentition. J Periodont, 59(8), Alaluusua, S., Saarela, M., Jousimies-Somer, H., & Asikainen, S. (1993). Ribotyping shows intrafamilial similarity in Actinobacillus actinomycetemcomitans isolates. Oral Microbiol and Immunol, 8(4), Albandar, J. M., Brown, L. J., & Löe, H. (1997). Putative periodontal pathogens in subgingival plaque of young adults with and without early-onset periodontitis. J Periodont, 68(10),

25 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited Ashbee, H. R., & Bignell, E. M. (2009). Pathogenic yeasts. [electronic resource]: Berlin ; London : Springer, Asikainen, S., Chen, C., & Slots, J. (1996). Likelihood of transmitting Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in families with periodontitis. Oral Microbiol and Immunol, 11(6), Batista, G. C. M., Krebs, V. L. J., Ruiz, L. S., Auler, M. E., Hahn, R. C., & Paula, C. R. (2014). Oral colonization: A possible source for candidemia in low-weight neonates. 24(2), 81. Berkowitz, R. J., & Jordan, H. V. (1975). Similarity of bacteriocins of Streptococcus mutans from mother and infant. Archiv Oral Biol, 20, Berkowitz, R. J., Jordan, H. V., & White, G. (1975). The early establishment of Streptococcus mutans in the mouths of infants. Archiv Oral Biol, 20(3), Bradshaw, D. J., Marsh, P. D., Watson, G. K., & Allison, C. (1998). Role of Fusobacterium nucleatum and Coaggregation in Anaerobe Survival in Planktonic and Biofilm Oral Microbial Communities during Aeration. Infect Immun, 66(10), Carlsson, J., Grahnén, H., & Jonsson, G. (1975). Lactobacilli and Streptococci in the Mouth of Children. Caries Res, 9(5), 333. Chen, H., & Jiang, W. (2014). Application of highthroughput sequencing in understanding human oral microbiome related with health and disease. Frontiers In Microbiology, 5, Christersson, L. A. (1993). Actinobacillus actinomycetemcomitans and localized juvenile periodontitis. Clinical, microbiologic and histologic studies. Swedish Dental Journal. Supplement, 90, Cortelli, J. R., Aquino, D. R., Cortelli, S. C., Nobre Franco, G. C., Fernandes, C. B., Roman-Torres, C. V. G., & Costa, F. O. (2008). Detection of Periodontal Pathogens in Oral Mucous Membranes of Edentulous Individuals. J Periodont, 79(10), Costerton, J. W., Lewandowski, Z., DeBeer, D., Caldwell, D., Korber, D., & James, G. (1994). Biofilms, the customized microniche. J Bacteriol, 176(8), Delaney, J. E., Ratzan, S. K., & Kornman, K. S. (1986). Subgingival microbiota associated with puberty: studies of pre-, circum-, and postpubertal human females. Paed Dent, 8(4), Ellen, R. P. (1976). Establishment and distribution of Actinomyces viscosus and Actinomyces naeslundii in the human oral cavity. Infect Immun, 14(5), Fives-Taylor, P. M., Meyer, D. H., Mintz, K. P., & Brissette, C. (1999). Virulence factors of Actinobacillus actinomycetemcomitans. Periodontol 2000, 20, Frandsen, E. V., Reinholdt, J., Kjeldsen, M., & Kilian, M. (1995). In vivo cleavage of immunoglobulin A1 by immunoglobulin A1 proteases from Prevotella and Capnocytophaga species. Oral Microbiol and Immunol, 10(5), Frisken, K. W., Higgins, T., & Palmer, J. M. (1990). The incidence of periodontopathic microorganisms in young children. [Article]. Oral Microbiol & Immunol, 5(1), doi: / X.ep Han, N., Xiao, X., Zhang, L., Ri, X., Zhang, J., Tong, Y., Xiao, Z. (1991). Bacteriological study of juvenile periodontitis in China. J Periodont Res, 26(5), Handley, P., Carter, P, Fielding, J. (1984). Streptococcus salivarius strains carry either fibrils or fimbriae on the cell surface. J Bacteriol (157), Handley, P., Carter, P, Wyett, JE, Hesketh, L. (1985). Surface structures (peritrichous fibrils and tufts of fibrils) found on Streptococcus sanguis strains may be related to their ability to coaggregate with other oral genera. Infect Immun 47, Haubek, D., Ennibi, O. K., Poulsen, K., Vaeth, M., Poulsen, S., & Kilian, M. (2008). Risk of aggressive periodontitis in adolescent carriers of the JP2 clone of Aggregatibacter (Actinobacillus) actinomycetemcomitans in Morocco: a prospective longitudinal cohort study. Lancet, 371(9608), Kilian, M., Reinholdt, J., Lomholt, H., Poulsen, K., & Frandsen, E. V. (1996). Biological significance of IgA1 proteases in bacterial colonization and pathogenesis: critical evaluation of experimental evidence. APMIS: Acta Pathologica, Microbiologica, Et Immunologica Scandinavica, 104(5), Kleinegger, C. L., Lockhart, S. R., Vargas, K., & Soll, D. R. (1996). Frequency, intensity, species, and strains of oral Candida vary as a function of host age. J Clin Microbiol, 34(9), Köhler, B., Lundberg, A.-B., Birkhed, D., & Papapanou, P. N. (2003). Longitudinal study of intrafamilial mutans streptococci ribotypes. Europ J Oral Sci, 111(5),

26 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited Kolenbrander, P. E. (2000). Oral Microbial Communities: Biofilms, Interactions, and Genetic Systems. [Article]. Ann Rev Microbiol, 54(1), 413. Kolenbrander, P. E., & Andersen, R. N. (1986). Multigeneric aggregations among oral bacteria: a network of independent cell-to-cell interactions. J Bacteriol, 168(2), Kolenbrander, P. E., Andersen, R. N., & Moore, L. V. (1990). Intrageneric coaggregation among strains of human oral bacteria: potential role in primary colonization of the tooth surface. Applied And Environmental Microbiol, 56(12), Kolenbrander, P. E., & London, J. (1993). Adhere today, here tomorrow: oral bacterial adherence. J Bacteriol (11-12), Könönen, E. (2000). Development of oral bacterial flora in young children. Annals of Medicine, 32(2), Könönen, E. (2005). Anaerobes in the upper respiratory tract in infancy. Anaerobe(3), 131. Könönen, E., Asikainen, S., & Jousimies-Somer, S. H. (1992). The early colonization of gram-negative anaerobic bacteria in edentulous infants. Oral Microbiol & Immunol, 7(1), Könönen, E., Asikainen, S., Saarela, M., Karjalalnen, J., & Jousimies-Somer, H. (1994). The oral gram-negative anaerobic microflora in young children: longitudinal changes from edentulous to dentate mouth. Oral Microbiol & Immunol, 9(3), Könönen, E., Jousimies-Somer, H., & Asikainen, S. (1992). Relationship between oral gram-negative anaerobic bacteria in saliva of the mother and the colonization of her edentulous infant. Oral Microbiol & Immunol, 7(5), Könönen, E., Kanervo, A., Takala, A., Asikainen, S., & Jousimies-Somer, H. (1999). Establishment of oral anaerobes during the first year of life. J Dent Res, 78(10), Könönen, E., & Muller, H. P. (2014). Microbiology of aggressive periodontitis. Periodontol 2000, 65(1), Könönen, E., Saarela, M., Karjalainen, J., Jousimies-Somer, H., Alaluusua, S., & Asikainen, S. (1994). Transmission of oral Prevotella melaninogenica between a mother and her young child. Oral Microbiol and Immunol, 9(5), Lamell, C. W., Griffen, A. L., McClellan, D. L., & Leys, E. J. (2000). Acquisition and colonization stability of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in children. J Clin Microbiol, 38(3), Lang, N. P., Bartold, P. M., Cullinan, M., Jeffcoat, M., Mombelli, A., Murakami, S., Dyke, T. V. (1999). Consensus Report: Aggressive Periodontitis. Law, V., Seow, W. K., & Townsend, G. (2007). Factors influencing oral colonization of mutans streptococci in young children. Aust Dent J, 52(2), López, N. J., Mellado, J. C., & Leighton, G. X. (1996). Occurrence of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia in juvenile periodontitis. J Clin Periodont, 23(2), Makhoul, I. R., Sujov, P., Ardekian, L., Kassis, I., Smolkin, T., Abu-Elnaa j, I., Laufer, D. (2002). Factors influencing oral colonization in premature infants. The Israel Med Assoc J: IMAJ, 4(2), Marsh, P. D. (2000). Role of the Oral Microflora in Health. [Article]. Microbial Ecol Health & Dis, 12(3), Marsh, P. D., & Bradshaw, D. J. (1995). Dental plaque as a biofilm. J Ind Microbiol, 15(3), Marsh, P. D., Head, D. A., & Devine, D. A. (2015). Dental plaque as a biofilm and a microbial community Implications for treatment. J Oral Biosci, 57(4), 185. Masuda, N., Shimamoto, T., Kitamura, K., Sobue, S., & Hamada, S. (1985). Transmission of Streptococcus mutans in some selected families. Microbios, 44(181S), Masunaga, H., Matsue, M., Matsue, I., Hirasawa, M., Takeuchi, T., & Ikeda, T. (1990). Microbiological study in clinically characterized rapidly progressive periodontal disease. Nihon Shishubyo Gakkai kaishi, 32(1), Matto, J., Saarela, M., Alaluusua, S., Oja, V., Jousimies- Somer, H., & Asikainen, S. (1998). Detection of Porphyromonas gingivalis from saliva by PCR by using a simple sample-processing method. J Clin Microbiol, 36(1), McCarthy, C., Snyder, M. L., & Parker, R. B. (1965). The indigenous oral flora of man. I. The newborn to the 1 year old infant. Archiv Oral Biol, 10, McClellan, D. L., Griffen, A. L., & Leys, E. J. (1996). Age and prevalence of Porphyromonas gingivalis in children. J Clin Microbiol, 34(8),

27 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited Mikx, F. H. M., Matee, M. I., & Schaeken, M. J. M. (1986). The prevalence of spirochetes in the subgingival microbiota of Tanzanian and Dutch children. 13(4), 289. Mombelli, A., Rutar, A., & Lang, N. P. (1995). Correlation of the periodontal status 6 years after puberty with clinical and microbiological conditions during puberty. J Clin Periodontol, 22(4), Moore, W., Holdeman, L., Smibert, R., Hash, D., Burmeister, J., & Ranney, R. (1982). Bacteriology of severe periodontitis in young adult humans. Infect Immun, 38(3), Moore, W. E., Burmeister, J. A., Brooks, C. N., Ranney, R. R., Hinkelmann, K. H., Schieken, R. M., & Moore, L. V. (1993). Investigation of the influences of puberty, genetics, and environment on the composition of subgingival periodontal floras. Infect Immun, 61(7), Moore, W. E., Holdeman, L. V., Smibert, R. M., Cato, E. P., Burmeister, J. A., Palcanis, K. G., & Ranney, R. R. (1984). Bacteriology of experimental gingivitis in children. Infect Immun, 46(1), 1-6. Morinushi, T., Lopatin, D. E., Van Poperin, N., & Ueda, Y. (2000). The relationship between gingivitis and colonization by Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans in children. J Periodont, 71(3), Nakagawa, S., Machida, Y., Nakagawa, T., Fujii, H., Yamada, S., Takazoe, I., & Okuda, K. (1994). Infection by Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, and antibody responses at different ages in humans. J Periodont Res, 29(1), Newman, M. G., Takei, H. H., Klokkevold, P. R., & Carranza, F. A. (2012). Carranza s clin periodont: St. Louis, MO : Saunders Elsevier, c th ed. Nishimura, F., Nagai, A., Kurimoto, K., Isoshima, O., Takashiba, S., & Kobayashi, M. (1990). A family study of a mother and daughter with increased susceptibility to early-onset periodontitis: microbiological, immunological, host defensive, and genetic analyses. J Periodont, 61(12), Papaioannou, W., Gizani, S., Haffajee, A. D., Quirynen, M., Mamai-Homata, E., & Papagiannoulis, L. (2009). The microbiota on different oral surfaces in healthy children. Oral Microbiol and Immunol(3), 183. Pearce, C., Bowden, G. H., Evans, M., Fitzsimmons, S. P., Johnson, J., Sheridan, M. J., & Cole, M. F. (1995). Identification of pioneer viridans streptococci in the oral cavity of human neonates. J Med Microbiol, 42(1), Pfaller, M. A., Jones, R. N., Messer, S. A., Edmond, M. B., & Wenzel, R. P. (1998). National surveillance of nosocomial blood stream infection due to species of Candida other than Candida albicans: frequency of occurrence and antifungal susceptibility in the SCOPE Program. SCOPE Participant Group. Surveillance and Control of Pathogens of Epidemiologic. Diagnostic Microbiol Infectious Dis, 30(2), Rosan, B., Slots, J., Lamont, R. J., Listgarten, M. A., & Nelson, G. M. (1988). Actinobacillus actinomycetemcomitans fimbriae. Oral Microbiol and Immunol, 3(2), Rotimi, V. O., & Duerden, B. I. (1981). The development of the bacterial flora in normal neonates. J Med Microbiol, 14(1), Rozkiewicz, D., Daniluk, T., Zaremba, M. L., Cylwik-Rokicka, D., Stokowska, W., Pawiska, M., & Waszkiel, D. (2006). Oral Candida albicans carriage in healthy preschool and school children. Adv In Med Sci, 51 Suppl 1, Ruby, J., & Goldner, M. (2007). Nature of symbiosis in oral disease. J Dent Res, 86(1), Sánchez-Vargas, L. O., Ortiz-López, N. G., Villar, M., Moragues, M. D., Aguirre, J. M., Cashat-Cruz, M.,... Quindós, G. (2005). Point prevalence, microbiology and antifungal susceptibility patterns of oral Candida isolates colonizing or infecting Mexican HIV/AIDS patients and healthy persons. Revista Iberoamericana De Micologí a, 22(2), Savitt, E. D., & Kent, R. L. (1991). Distribution of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis by subject age. J Periodont, 62(8), Slots, J. (1976). The predominant cultivable organisms in juvenile periodontitis. Euro J Oral Sciences, 84(1), Slots, J., Reynolds, H. S., & Genco, R. J. (1980). Actinobacillus actinomycetemcomitans in human periodontal disease: a cross-sectional microbiological investigation. Infect Immun, 29(3), Smith, D. J., Anderson, J. M., King, W. F., van Houte, J., & Taubman, M. A. (1993). Oral Streptococcal colonization of infants. Oral Microbiol & Immunol, 8(1), 1-4. doi: / X.ep Socransky, S., & Haffajee, A. (2005). Periodontal microbial ecology. [Article]. Periodontol 2000, 38(1),

28 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited Socransky, S., Kaffajee, A. D., Cugini, M. A., Smith, C., Kent, R. L., & Jr. (1998). Microbial complexes in subgingival plaque. J Clin Periodontol, 25(2), Socransky, S., & Manganiello, S. D. (1971). The oral microbiota of man from birth to senility. J Periodont, 42(8), Tanner, A. C. R., Milgrom, P. M., Kent, R., Jr., Mokeem, S. A., Page, R. C., Riedy, C. A., & Bruss, J. (2002). The microbiota of young children from tooth and tongue samples. J Dent Res, 81(1), Ting, M., Contreras, A., & Slots, J. (2000). Herpesviruses in localized juvenile periodontitis. J Periodont Res, 35(1), Umeda, M., Miwa, Z., Takeuchi, Y., Ishizuka, M., Huang, Y., Noguchi, K., & Ishikawa, I. (2004). The distribution of periodontopathic bacteria among Japanese children and their parents. J Periodont Res, 39(6), van Oosten, M. A., Mombelli, A., Gusberti, F. A., & Lang, N. P. (1988). Black-pigmented Bacteroides and spirochetes in the subgingival microbiota of prepubertal schoolchildren. J Periodont Res, 23(3), Vandesteen, G. E., Williams, B. L., Ebersole, J. L., Altman, L. C., & Page, R. C. (1984). Clinical, microbiological and immunological studies of a family with a high prevalence of early-onset periodontitis. J Periodontol, 55(3), Wade, W. G. (2013). The oral microbiome in health and disease. Pharmacol Res, 69(1), Waggoner-Fountain, L. A., Walker, M. W., Hollis, R. J., Pfaller, M. A., Ferguson, J. E., 2nd, Wenzel, R. P., & Donowitz, L. G. (1996). Vertical and horizontal transmission of unique Candida species to premature newborns. Clin Infect Dis, 22(5), Walsh, L. J. (2009). Microbiology Retrieved from espace.library.uq.edu.au/view/uq:256309/racds_micro_ book_2009_march18.pdf Whittaker, C. J., & Klier, C. M. (1996). Mechanism of adhesion by oral bacteria. [Article]. Ann Rev Microbiol, 50(1), 513. Williams, B. L., Ebersole, J. L., Spektor, M. D., & Page, R. C. (1985). Assessment of serum antibody patterns and analysis of subgingival microflora of members of a family with a high prevalence of early-onset periodontitis. Infect Immun, 49(3), Williams, R., & Gibbons, R. (1972). Inhibition of bacterial adherence by secretory immunoglobulin A: a mechanism of antigen disposal. Science, 177(4050), Wojcicki, C. J., Harper, D. S., & Robinson, P. J. (1987). Differences in periodontal disease-associated microorganisms of subgingival plaque in prepubertal, pubertal and postpubertal children. J Periodontol, 58(4), Yang, E. Y., Tanner, A. C. R., Milgrom, P., Mokeem, S. A., Riedy, C. A., Spadafora, A. T., & Bruss, J. (2002). Periodontal pathogen detection in gingiva/tooth and tongue flora samples from 18- to 48-month-old children and periodontal status of their mothers. [Article]. Oral Microbiol & Immunol, 17(1), Yoshimura, F., Takahashi, K, Nodaska, Y, Susuki, T. (1984). Purification and characterisation of a novel type of fimbriae from the oral anaerobe Bacteroides gingivalis. J Bacteriol, 160, Zambon, J. J. (1985). Actinobacillus actinomycetemcomitans in human periodontal disease. J Clin Periodontol, 12(1), Zambon, J. J., Christersson, L. A., & Slots, J. (1983). Actinobacillus actinomycetemcomitans in human periodontal disease. Prevalence in patient groups and distribution of biotypes and serotypes within families. J Periodontol, 54(12),

29 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited Dental Implant Screw Mechanics Louis Kei, Iven Klineberg Introduction The use of implant-supported single crowns and implantsupported fixed dental prostheses have gained popularity in the last 2 decades. Despite considered as a safe and effective treatment modality, technical complications such as abutment screw or prosthetic screw loosening and fracture remain a common problem(1). The aim of this article is to review the latest literature on implant screw mechanics, factors that affect screw joint stability, practical solutions that limit screw loosening or fracture, and techniques on the removal of fractured abutment screws. Implant screw mechanics An implant screw joint can be considered as 2 parts the implant fixture and the abutment, or between the abutment and the dental prosthesis; tightened together by a screw as described by McGlumphy and colleagues(2). The screw is tightened by applying torque. As the screw is tightened, it elongates, producing a tensile force. This tensile force is commonly referred to as the preload(2). The preload is what keeps the screw threads tightly secured to the mating counterpart within the implant fixture and holds the fixture and abutment together by producing a clamping force between the screw head and its seat. The proload produced within an implant screw joint is generally directly proportional to the tightening torque(2). The manufacturer usually recommends a specific torque for each screw/abutment assembly of which is dictated by the material and design of the specific screw joint. Clinically, the implant screw joint is constantly subjected to external joint- separating forces within the oral cavity that may include the following: Excursive contacts Off-axis centric contacts Interproximal contacts Cantilever contacts Non-passive framework of a dental prosthesis Abstract: Purpose: Technical complications such as abutment/ prosthetic screw loosening or fracture may occur to implant supported restorations. The aim of this article is to review the scientific literature on implant screw mechanics. Method: A search of the English language peerreviewed literature on implant screw mechanics using Medline and Google Scholar for the period of 1990 to 2016 was completed. Results: A range of factors have been identified that may affect implant screw joint stability. These include the preload, embedment relaxation, screw material and coating, screw design, abutment-implant interface design, abutment-implant interface misfit, functional forces, implant diameter, number of implants, passive fit of prosthesis, torque wrench, repeated opening and closing of the screws, and splinting versus nonsplinting adjacent implants. Practical measures to limit screw loosening and fracture were discussed, as well as techniques to retrieve a fractured screw. Conclusion: Implant-supported restorations have gained widespread popularity in the replacement of missing teeth. However, abutment and prosthetic screw loosening and fracture remain a common occurrence. This article has reviewed the contemporary literature on dental implant screw mechanics and has summarized key factors that contribute to implant screw joint stability, practice measures to minimize screw joint loosening and techniques on retrieving fractured abutment screws. Keywords: implant screw, preload, screw loosening, screw retrieval. 27

30 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited The screw loosens if outside forces trying to separate the parts are greater than the preload within the screw joint. Excessive joint separating forces causes slippage between threads of the screw and threads of the bore, resulting in a loss of preload. When preload is lost, micro-motions within the screw joint increases dramatically during function. The anti-rotational features of the abutment implant interface cease to engage properly and the protection it offers to the screw against excessive external forces is lost. When the external forces exceed the yield strength of the screw, the screw plastically deforms and may fracture as a result. Factors that may affect implant screw joint stability Preload McGlumphy and colleagues recommended in order to maximise screw joint stability, maximum clamping forces (preload) should be generated(2). The ideal preload for a particular screw was recommended at 75% of the yield strength of the screw material(2). Martin et al demonstrated in their lab-based study that in general, the more torque applied to an abutment screw, more preload is achieved within the screw joint assembly(3). Haack and colleagues discovered applying manufacturer s recommenced tightening torques in 2 commercially available abutment screws were well within its elastic range, and suggested tightening the screws beyond recommended levels may be possible without producing plastic deformation whilst reducing the risk of screw loosening(4). Embedment relaxation (Settling effect) Embedment relaxation or the settling effect of screw joints depicts the phenomenon whereby a significant loss of preload was observed after the screw was initially tightened into place within the joint assembly. This is based on the fact that no surface is completely smooth. Even a carefully machined implant or screw surface is slightly rough when viewed microscopically. Because of this micro-roughness, no two surfaces are completely in contact with one another. When the screw joint assembly is subjected to external loads subsequently, wear of the contact areas ensue, bringing the two surfaces closer to each other. As a result of this, a loss of preload follows. It has been reported in the literature that 2%-10% of the initial preload is lost to embedment relaxation of the screw joint assembly(4-7). The magnitude of settling depends on the initial surface roughness, surface hardness, as well as the magnitude of loading forces. Jorneus et al demonstrated in their in-vitro study a significant loss of reverse torque (proxy for preload) was observed in 4 types of abutment screws made from various alloys(6). Siamos and colleagues observed a decrease of up to 29% of torque in implant joint assemblies after 3 hours from the initial tightening. However, when the abutment screws were retightened after 10 minutes from the initial tightening, the torque loss after 3 hours reduced to only 19%(7). Screw material and coating The material of which the abutment or prosthetic screw is fabricated from directly influences the amount of preload that can be generated within the screw joint assembly. For instance, a material that has a high yield strength that can tolerate a high insertion torque may accommodate a higher preload within the implant joint assembly. Jorneus and collagues compared the torque generated from 3 screws fabricated from different metal alloys and concluded that the gold alloy screw produced the highest preload (as oppose to 2 other types of titanium alloy screws)(6). In the last decade, implant manufacturers experimented adding a solid lubricant on abutment screw surfaces to decrease the coefficient of friction. It is thought that a reduction in the surface friction may reduce the embedment relaxation of the screw joint, therefore achieving higher preloads and better joint stability. Examples of solid lubricants include: Gold-Tite - Gold alloy screw (80% Pd, 10% Ga, 10% Cu/Au/Zn) coated with 0.76um of pure gold (3i Implant Innovations, Inc.)(3, 8) TorqTite - Titanium alloy screw coated with amorphous carbon (Nobel Biocare)(5, 8) TiCN coating(9) TiN coating(3) Parylene N coating(9) Teflon coating(9) Martin and colleagues evaluated the materials and surfaces of four commercially available abutment screws on preload generation and found the greatest preload values at 20Ncm and 32Ncm were by the Gold-Tite and TorqTite abutment screws (as oppose to non-coated gold alloy and titanium alloy screws)(3). Byrne et al compared three screws (titanium alloy, gold alloy, and gold-coated gold alloy) with similar geometry by recording the preload induced when various torques were 28

31 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited used for fixation. They found the gold-coated screw showed markedly higher preloads for all insertion torques and for all instances of tightening when compared with the uncoated screws(8). On the contrary, Elias and colleagues compared the preload generated by screws coated with four solid lubriants (TiN, TiCN, Parylene N, and Teflon coating) with an uncoated titanium alloy abutment screw. It was found that at insertion torque below 30Ncm, the coated-screws generally performed better than the uncoated control, whilst at torque >30Ncm, the uncoated titanium screw produced higher preloads than its coated counterparts(9). The authors recommended each clinician should double check the specific preload data of the new coated-screws prior to its use. Screw design Jorneus et al compared the preload generated by 2 abutment screw head designs (flat head and conical head) and found a significantly lower preload was generated with abutment screws having a conical head design. The authors speculated that the conical screw lost a major part of the torque as friction between the conical screw head and the abutment, thereby allowing less preload generated within the screw joint assembly(6). A retrospective study of 50 patients with implant-retained and -supported fixed dental prostheses of at least 5 years by Kallus and Bessing discovered that gold prosthetic screws with an internal hexagon screw heads were more frequently tight than those with slot head designs(10). The authors speculated it was more difficult to apply manual force when tightening a slotted screw because of the clinician s anxiety concerning driver slippage from the slot. Abutment / Implant interface misfit The abutment / implant interface misfit has been considered a significant factor in screw joint failure. Binon evaluated the machining accuracy and consistency of 13 implants having external hexagonal extensions and investigated the rotational freedom between the patrix implant hexagonal extension and the matrix hexagonal abutment counterpart(11). The author found a considerable variation in accuracy and consistency amongst different implant systems. The degrees of rotation of the abutment over the implant fixture a proxy for abutment/implant interface misfit, were found to range from 1.4 degrees to 10.1 degrees amongst the various implant systems. The author concluded a rotation of less than 5 degrees is desirable for optimal screw joint stability. In another laboratory study by Binon, a series of 10 incrementally larger UCLA abutments were loaded off axis with 133N and cycled at 1150 vertical strokes per minute(12). Rotational misfit between internal and external hexagons ranged from 1.94 degrees for the smallest abutment to degrees for the largest. It was found there was a strong direct correlation between the amount of hexagonal misfit and screw loosening. The authors concluded the greater the rotational freedom, the greater the probability of screw loosening. Abutment / Implant interface design The anti-rotational element offered by the abutment/implant interface design is crucial in the preservation of the abutment screw preload during function. When functional forces are applied onto the implant crown/abutment assembly, a welldesigned A/I interface can significantly reduce the amount of joint separating forces transferred onto the abutment screw, reducing the chances of abutment screw loosening or fracture. Binon removed the external hex from the implant fixture and subjected the implant-abutment assembly to simulated functional loading. It was found the absence of the external implant hex extension significantly increases the likelihood to screw loosening(12). Khraisat et al investigated the effect of lateral cyclic loading on abutment screw loosening of an external hexagon implant system(13). The authors discovered that external forces that trigger a better engagement the external hex of the implant abutment interface (less micro-movements between the abutment and fixture), the preload of the abutment screw were better preserved than those implants that were subjected to direct horizontal loads (increased micro-movements). Weiss and colleagues recorded repeated opening torque values of 7 commercially available implant/abutment assemblies and found systems with morse tapered and spline connections consistently maintained a higher preload values than the external hex connections(14). Functional forces McGlumphy and colleagues proposed the following strategies to minimize joint separating forces to the implant abutment assembly(2): Minimise prosthesis cantelever Minimise contacts in lateral excursion Minimise off-axis centric contacts Reduce cuspal angles 29

32 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited Bakaeen et al investigated influence of the buccolingual width of the occlusal table on the untightening torque required to loosen gold prosthetic screws after subjecting implants and implant-supported restorations to simulated occlusal loads(15). The authors discovered a significant reduction in screw untightening torque (proxy for a higher loss of preload) in the restorations with a wide occlusal table compared to restorations with a narrow occlusal table. Diameter of implant Boggan and colleagues conducted a laboratory study on the influence of implant platform diameter on the mechanical strength and quality of fit of the implantabutment interface(16). Static and cyclic compressive bending tests were conducted on 4mm and 5mm diameter implants. Failure mode for static test samples was bending or deformation of the abutment screw, where as fracture of the abutment screw was the common failure mode for the fatigue test samples. The 5mm diameter implant was stronger in both static and fatigue conditions than the 4mm diameter implants. Number of implants Bakaeen and colleagues compared the incidence of screw loosening and values of untightening torque of the screws among crowns supported by 1 wide-diameter as opposed to 2 standard implants after loading in vitro(15). The crowns were subjected to a 6-kg load for cycles over 5.5 hours and were loaded at the outer and inner inclines and cusp tips. The authors found restoring missing molars with 1 wide-diameter implant had a greater incidence of screw loosening as compared with 2 implants. Passive fit of prosthesis In a retrospective study by Kallus and Bessing, patients restored with implant-retained and -supported fixed dental prostheses were more likely to have gold prosthetic screw loosening when their prosthesis was judged to have a misfit between the framework and the abutments by a calibrated examiner(10). Torque wrench The appropriate amount of torque applied to the abutment/ prosthetic screw by the clinician is crucial to the long-term implant joint stability. Inadequate tightening may cause premature loosening of the screw whilst in function, yet excessive torque that exceeds the yield strength of the screw will create permanent deformation in the screw shank, leading to screw fracture. Gutierrez et al tested the accuracy of torque delivery of 35 detent joint implant torque wrenches that has been in clinical service between 1 month to 3 years(17). These torque wrenches were engineered to be accurate within a margin of error of +/- 3%. The authors discovered of the 35 torque wrenches tested, 25 produced a torque that was high, 5 low and only 6 of them were within the 3% limit. The biggest error recorded was 455% greater than the intended 10Ncm the torque wrench was suppose to deliver. Severe corrosion of the spring was discovered when the offending torque wrench was dissembled. Repeated opening and closing During impression and prosthesis fabrication, repeated closing and opening of abutment screws may cause component wear and decrease frictional fit of the mating parts, resulting in altered resistance to opening and potential loss of preload in function. Weiss and colleagues compared torque loss as a result of multiple consecutive closures within and between 7 commercially available implant systems(14). Repeated opening-closing cycles were used to simulate in-vitro embedment relaxation and component wear. Screw opening torque values were recorded up to 200 consecutive closures at 20Ncm. A progressive decrease in opening torque values was measured in all implant systems. Percentage torque loss ranged from 3%-20% on immediate opening, and from 4.5%-36% for average of first 30 openings. The authors concluded that the reduction in opening torque was probably due to a decrease in the coefficient of friction between the mating components. Byrne et al measured the preloads generated with repeated tightening in 3 types of screwed used in dental implant assemblies (Titanium alloy, Gold alloy, Gold-coated)(8). All screws showed decay in preload with the number of times tightened, with the gold-coated screw losing more preload on the second and third tightenings than either of the uncoated screw. The authors speculated the gold coatings on the Gold-Tite screw may be damaged during insertion, therefore the coating is less effective on subsequent insertions in generating the high preloads it achieved in the first tightening. On the contrary, Tzenakis and colleagues evaluated the effect of repeated preload torque and salivary contamination on the preload of slotted gold implant prosthetic screws(18). 30

33 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited Higher preloads were achieved after repeated opening and closing of up to 10 times to 10Ncm. The authors speculated the repeated opening and closing of the screw joint resulted in a gradual elimination of micro-roughness of the mating surfaces, permitted a better and smoother contact between the surfaces, and hence more torquing force was transformed into preload. Splinting vs non-splinting adjacent implants Clelland and colleagues conducted a split-mouth prospective controlled trial to investigate complications of splinted and non-splinted short adjacent implants in the posterior segment for up to 3 years(19). Eighteen patients who required bilateral consecutive implants were restored with non-splinted implant crowns on one side and the contralateral side with splinted fixed prosthesis. Screw loosening was found to be the main prosthetic complication, with all screw loosening only occurring on the non-splinted side for 5 of 15 patients. Practical measures to limit screw loosening / fracture Table 1 contains a host of practical recommendations to limit implant screw loosening or fracture: Table 1. Practical Measures To Limit Implant Screw Loosening and/or Fracture Screw selection Screw tightening Abutment / Implant connection selection Prosthesis design Implant selection Occlusal design Torque wrench Use genuine manufacturer-supplied abutment and prosthetic screws to ensure quality and consistency Use gold-coated abutment screw if high preload is required Avoid using newer solid-lubricant-coated screws until reliable published data confirms higher preload can be achieved with these screws Avoid using conical-shaped head abutment screws Select internal hexagon prosthetic screws where possible over slotted prosthetic screws Use a brand new screw for the delivery of a new prosthesis (Avoid allowing the lab to use the new screw for the fabrication of the restoration) Apply the manufacturer recommended torque values Retorque the abutment / prosthetic screw after 10 minutes from the initial tightening to minimize preload loss due to embedment relaxation Minimise unnecessary opening and closing of abutment / prosthetic screws, especially when a gold coated screw is selected Use reputable implant manufacturers to ensure high quality and precisely machined A/I fit In cases with expected high occlusal loads, select an A/I interface that offers superior anti-rotational features for better abutment screw protection (i.e. high external hex height, spline connections) Minimise cantelever Ensure passive framework fit Splint adjacent implants Use a wide platform implant in posterior regions Use 2x regular neck implants to replace a large molar if possible Minimise excursive contacts Minimise off-axis centric contacts Reduce cusp height and angles Reduce width of occlusal table Annual calibration to ensure accurate torque output of the torque wrench Inspection for any corrosion in the spring component in detent joint wrenches 31

34 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited Techniques of retrieving a fractured screw The Ultrasonic Scaler Technique(20) 1. An access hole was made occlusally through the crown to access the screw head 2. Retrieve the crown along with the abutment 3. Once the crown and abutment were removed, a radiograph was taken to reconfirm the fractured part of the abutment screw inside the implant 4. A fine tapered carbide bur is used to make a notch on the occlusal surface of abutment screw between the center of the screw and its periphery. Care is taken not to touch the internal threads of the implant with the bur, and at the same time the notch is not at the center 5. An ultrasonic scaler tip is then inserted into the implant and is made to engage the notch created 6. The ultrasonic scaler is started at a very low speed, and mechanically the tip of the scaler is moved counterclockwise to remove the fractured screw The Self-Made Screw Driver Technique(21) 1. A flame-shaped bur is modified to prepare a groove on the fractured screw. The diamond particles of the upper part of the flame-shaped bur are removed and polished in order not to damage the internal screw thread of the implant 2. A thin groove was created on the screw piece 3. A handmade screwdriver is prepared from a detrited tungsten carbide bur. The upper part of the bur is cut to the desired length. The tip of the bur is made thin (1.5mm in width) and sharpened as a screwdriver with ah carbon separating disc 4. An angular-shaped handhold is made from autoplymerising acrylic resin to hold and rotate the screwdriver easily 5. The handmade screwdriver is positioned onto the groove that is prepared in the fractured screw in the implant and slowly rotated counter clockwise Conclusion Dental implant-supported restorations have gained popularity in the replacement of missing teeth. However, abutment and prosthetic screw loosening and fracture remain a common occurrence. This article has reviewed the contemporary literature on dental implant screw mechanics and has summarized the key factors that contribute to implant screw joint stability, practical measures to minimize screw joint loosening and techniques on retrieving fractured abutment screws. References 1. Albrektsson T, Donos N, Working G. Implant survival and complications. The Third EAO consensus conference Clinical oral implants research. 2012;23 Suppl 6: McGlumphy EA, Mendel DA, Holloway JA. Implant Screw Mechanics. Dent Clin N Am. 1998;42: Martin WC, Woody RD, Miller BH, Miller AW. Implant abutment screw rotations and preloads for four different screw materials and surfaces. J Prosthet Dent. 2001;86(6): Haack JE, Sakaguchi RL, Sun T, Coffey JP. Elongation and preload stress in dental implant abutment screws. Int J Oral Maxillofac Implants. 1995;10: Winkler S, Ring K, Ring JD, Boberick KG. Implant screw mechanics and the settling effect: An overview. J Oral Implantol. 2003;29: Jorneus L, Jemt T, Carlsson L. Loads and designs of screw joints for single crowns supported by osseointegrated implants. Int J Oral Maxillofac Implants. 1992;7: Siamos G, Winkler S, Boberick KG. The relationship between implant preload and screw loosening on implantsupported prostheses. J Oral Implantol. 2002;28: Byrne D, Jacobs S, O Connell B, Houston F, Claffey N. Preloads generated with repeated tightening in three types of screws used in dental implant assemblies. J Prosthodont 2006;15: Elias CN, Figueira DC, Rios PR. Influence of the coating material on the loosing of dental implant abutment screw joints. Materials Science and Engineering. 2006;26: Kallus T, Bessing C. Loose gold screws frequently occur in full-arch fixed prostheses supported by osseointegrated implants after 5 years. Int J Oral Maxillofac Implants. 1994;9: Binon PP. Evaluation of machining accuracy and consistency of selected implants, standard abutments, and laboratory analogs. Int J Prosthodont. 1995;8:

35 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited 12. Binon PP. The effect of implant/abutment hexagonal misfit on screw joint stability. Int J Prosthodont. 1996;9: Khraisat A, Hashimoto A, Nomura S, Miyakawa O. Effect of lateral cyclic loading on abutment screw loosening of an external hexagon implant system. J Prosthet Dent. 2004;91(4): Weiss EI, Kozak D, Gross MD. Effect of repeated closures on opening torque values in seven abutmentimplant systems. J Prosthet Dent. 2000;84: Bakaeen LG, Winkler S, Neff PA. The effect of implant diameter, restoration design, and occlusal table variations on screw loosening of posterior single-tooth implant restorations. J Oral Implantol. 2001;27: Boggan RS, Strong JT, Misch CE, Bidez MW. Influence of hex geometry and prosthetic table width on static and fatigue strength of dental implants. J Prosthet Dent. 1999;82(4): Gutierrez J, Nicholls JI, Libman WJ, Butson TJ. Accuracy of the implant torque wrench following time in clinical service. Int J Prosthodont. 1997;17: Tzenakis GK, Nagy WW, Fournelle RA, Dhuru VB. The effect of repeated torque and salivary contamination on the preload of slotted gold implant prosthetic screws. J Prosthet Dent. 2002;88: Clelland N, Chaudhry J, Rashid RG, McGlumphy E. Split- Mouth Comparison of Splinted and Nonsplinted Prostheses on Short Implants: 3-Year Results. Int J Oral Maxillofac Implants. 2016;31(5): Walia MS, Arora S, Luthra R, Walia PK. Removal of fractured dental implant screw using a new technique: a case report. J Oral Implantol. 2012;38(6): Kurt M, Guler AU, Duran I. A technique for removal of a fractured implant abutment screw. J Oral Implantol. 2013;39(6): AOS PRESENTS HALF-DAY EVENT Proudly sponsored by AUSTRALIAN ROADSHOW BRISBANE Tuesday 17th October 2017 E: infoqld@aos.org.au Professor Tord Berglundh, Sweden. DDS, PhD Professor Department of Periodontology Institute of Odontology Sahlgrenska Academy University of Gothenburg. CURRENT CHALLENGES IN IMPLANT DENTISTRY. PERI-IMPLANTITIS - DIAGNOSIS, PREVALENCE, RISK FACTORS AND TREATMENT. COURSE OUTLINE Understanding outcomes in implant therapy Prevalence and risk factors for peri-implantitis Peri-implantitis and periodontitis - two different entities? Treatment of peri-implantitis IF YOU ARE PLACING IMPLANT AND ARE RESPONSIBLE FOR THEIR FUTURE CARE AND MAINTENANCE YOU NEED TO ATTEND SYDNEY Thursday 19th October 2017 E: infonsw@aos.org.au MELBOURNE Saturday 21st October 2017 E: infovic@aos.org.au PERTH Monday 23rd October 2017 E: rsarmidi@yahoo.com For details, pricing and registration please check the website 33

36 A VOLUME 1 Issue 1 June 2017 and Implant Dentistry Limited Australian Periodontology Research Foundation Report 2017 The APRF continues to enjoy and benefit from ongoing support from both the periodontal profession and the dental industry. A full list of sponsors is detailed within this report. A major activity of the Foundation is to support periodontal research in Australia. We are pleased to report the following current projects are supported by the APRF. Current APRF Sponsored Research Projects Haemolytic activity of bacteria in peri-implantitis Institute: University of Melbourne Investigators: F Chan, I Darby, N McGregor, H Butt Clinical and microbiologival evaluation of one stage full mouth disinfection in conjunction with systemically administered azithromycin: a randomised controlled clinical trial Institute: University of Western Australia Investigators: E Elhassan, A Quaranta, J Rincon The effect of different air-abrasive powders and delivery times on contaminated titanium implant surfaces: an in-vitro pilot study Institute: University of Western Australia Investigators: S Abd EL Nour, A Quaranta, A Tawse-Smith, K Shearston The effect of piezocision on periodontal parameters: A randomized controlled clinical split mouth study Institute: University of Sydney Investigators: S Madukuri, A Spahr, J Mahon, F Zahr Th17 cells in chronic periodontal disease Institute: University of Melbourne Investigators: N Medara, I Darby, N O Brien-Simpson, J Lenzo Adjunct use of photodynamic therapy in periodontitis patients with persisting pocklets, bleeding on probing and ongoing attachment loss Institute: University of Sydney Investigators: J Vo, A Spahr The effect of azithromycin on the treatment of peri-implant infection Institute: University of Sydney Investigators: L Gershenfeld, S Yeung, A Spahr The effect of azithromycin on the treatment of peri-implant infection Institute: University of Sydney Investigators: A Kalos, S Yeung 34

37 VOLUME 1 Issue 1 June 2017 A and Implant Dentistry Limited An evaluation of whole biofilm models on titanium implants: a proof of concept study Institute: University of Queensland Investigators: C Tran, L Walsh Efficacy of azithromycin compared with other antibiotics used in the clinical practice for the treatment of Aggregatibacter actinomycetemcomitans associated periodontal disease Institution: University of Melbourne Investigators: O Oettinger-Barak, S Dashper, I Darby APRF Student Publication Prize Each year the APRF awards a prize for the best postgraduate student paper published the previous year and presents the winner with a plaque at the next ANZAP or ASP meeting in recognition of their efforts. The winner of the prize for best paper published in 2015 was Dr Mohammed Alfarsi from Griffith University for the paper The effect of platelet proteins released in response to titanium implant surfaces on macrophage pro-inflammatory cytokine gene expression. Clin Implant Dent Relat Res 2015 Dec;17(6): The award was presented at the ANZAP meeting in Perth in March. Corporate Sponsor Acknowledgements In addition to per capita membership support from the Australian and New Zealand Academy of Periodontists and the Australian Society of Periodontology, the APRF very gratefully acknowledges the support of the following: Platinum Level - $10,000 per annum Colgate Oral Care Titanium Level - $3,000 per annum Dentsply Implants Nobel Biocare Silver Level - $2,000 per annum Straumann Bronze Level - $1,000 per annum Henry Schein Halas Website The APRF now has an online presence as part of the ASP website at Information on the APRF is available for download. 35

38 NovaBone Dental Putty Simple Delivery, Great Handling & Proven Results NovaBone is a fully synthetic bone substitute that aims to redefine minimally invasive bone grafting surgeries. Engineered for enhanced handling and improved performance, this next generation calcium phosphosilicate bone substitute is delivered through a proprietary uni-dose cartridge system (AUS) or (NZ) or 3iaus-nzorders@zimmerbiomet.com All references to Zimmer Biomet Dental contained herein refer to the dental subsidiaries of Zimmer Biomet Holdings, Inc. Unless otherwise indicated, as referenced herein, all trademarks are the property of Zimmer Biomet; and all products are manufactured, distributed and marketed by Zimmer Biomet Dental. NovaBone Dental Putty is manufactured by NovaBone Products, LLC. NovaBone is a registered trademark of NovaBone Products, LLC. For additional product information, please refer to the individual product labeling/ifu. Product clearance and availability may be limited to certain countries/regions. This material is intended for clinicians only and does not comprise medical advice or recommendations. This material may not be copied or reprinted without the express written consent of Zimmer Biomet. ZB0136AUS REV A 01/ Zimmer Biomet. All rights reserved.

39 VOLUME 1 Issue 1 June 2017 Australian Society of Periodontology State Branch News A ASP NSW President: Dr Joseph Lee Vice President: Dr Patty Chou Secretary/Treasurer: Dr Beth Kang State Branch Councillor: Dr Rajiv Verma Secretariat: Mrs Helen Mooney helen.mooney4@gmail.com Meeting 1: Meeting Name: March Meeting Meeting Date & Time: Thursday, 2 March 6:15 p.m. Pre-Dinner Drinks Meeting Location: Doltone House Hyde Park, 181 Elizabeth Street, Sydney Speaker: Dr Michelle Heffernan Topic: Clinical keys to determine the prognosis of a tooth Cost & Other Details: Visitors: $110 / Hygienists: $88 / Complimentary for Members Meeting 2: Meeting Name: May Meeting Meeting Date & Time: Thursday, 25 May :15 p.m. Pre-Dinner Drinks Meeting Location: Doltone House Hyde Park, 181 Elizabeth Street, Sydney Speaker: Dr Kevin Todes Topic: Soft Tissue Grafting Techniques Cost & Other Details: Visitors: $110 / Hygienists: $88 / Complimentary for Members Meeting 3: Meeting Name: July Meeting Meeting Date & Time: Thursday, 20 July :15 p.m. Pre-Dinner Drinks Meeting Location: Doltone House Hyde Park, 181 Elizabeth Street, Sydney Speaker: Prof. Sasso Ivanovski Topic: Tissue Engineering in Periodontics Cost & Other Details: Visitors: $110 / Hygienists: $88 / Complimentary for Members Meeting 4: Meeting Name: Full Day Seminar Meeting Date & Time: Friday, 3 November 2017 Registration from 7:00 for 8:00 a.m. start Meeting Location: Doltone House Hyde Park, 181 Elizabeth Street, Sydney Speaker: Dr Marco Esposito University of Goteborg, Sweden Topic: Implant Dentistry: An evidencebased overview Cost & Other Details: Non-Members: $390 / Non-Member Hygienists: $220 / Members/Students: $100 ASP SA President: Dr Danny Ho Vice President: Dr Brian Chee Secretary: Dr Rischelle Saviour Treasurer: Dr Geoff Harvey aspsa2@gmail.com Meeting 1: Meeting name: Seminar Meeting 1 Meeting date & time: 15th March :30 pm Meeting location: Farina 00, 128 King William Road, Goodwood SA 5034 Speakers: Dr Jessica O Neill, Periodontist Topics: Periodontal treatment considerations for the female patient Cost & other details: See below Meeting 2: Meeting name: Seminar Meeting 2 Meeting date & time: 3rd May :30 pm 37

40 A VOLUME 1 Issue 1 June 2017 Australian Society of Periodontology State Branch News ASP SA (continued) Meeting location: Gaucho s Argentinian Restaurant, 91 Gouger St, Adelaide SA 5000 Speakers: Dr Geraldine Moses, Pharmacist and Health Professional Educator Topics: An update on anticoagulants, antiplatelets, bisphosphonates and MRONJ drugs Cost & other details: See below Meeting 3: Meeting name: Seminar Meeting 3 Meeting date & time: 16th August :30 pm Meeting location: Hotel Tivoli, 265 Pirie St, Adelaide SA 5000 Speakers: Dr Robert Fell, Periodontist Topics: Implant treatment in periodontal patients: What are the challenges? Cost & other details: See below Meeting 4: Meeting name: Seminar Meeting 4 Meeting date & time: 1st November :30 pm Meeting location: Cos 18 Leigh, 18 Leigh St, Adelaide SA 5000 Speakers: Dr David Drew, Periodontist Topics: The Zen of periodontal maintenance Cost & other details: See below 2017 MEMBERSHIP Costs Dentist: $420 (includes 4 x dinner meetings, Federal membership) Dental Therapist, Hygienist: $350 (includes 4 x dinner meetings, Federal membership) Postgraduate Student, First Year Graduates: $350 (includes 4 x dinner meetings, Federal membership) Guest for Individual Dinner Meeting: $120 ASP WA President: Dr Amy Hope Secretary: Dr Anna Hughes Treasurer: Dr Ahmed Saleh State Branch Councillor: Dr Zahida Oakley aspwaperth@gmail.com Meeting 1: Meeting name: ASP WA Branch presentation Meeting date & time: May 30th pm Meeting location: ADA House, Havelock street, West Perth Speakers: Dr Bernard Koong Topics: Imaging the periodontium and related structures Cost & other details: Free for members Meeting 2: Meeting name: ASP WA Branch presentation/agm Meeting date & time: August 15th pm Meeting location: ADA House, Havelock street, West Perth Speakers: Prof Alex Quaranta and the perio postgrads Topics: Current research topics at UWA Cost & other details: Free for members Meeting 3: Meeting name: ASP WA Branch dinner meeting Meeting date & time: November 23rd pm Meeting location: TBA 38

41 VOLUME 1 Issue 1 June 2017 Australian Society of Periodontology State Branch News A ASP WA (continued) Speakers: Dr Geraldine Moses Topics: Pills and pockets ( to be confirmed) Cost & other details: Free for members $130 for non-members Meeting 4: Meeting name: ASP Biennial Meeting Meeting date & time: 8-10 March 2018 Meeting location: Perth Speakers: Professor Björn Klinge, Professor Gianni Salvi, Dr Jeanie Suvan, further speakers to be announced soon. Topics: Perio Power how dentistry can profit from periodontics Cost & other details: ASP QLD President: Dr Christopher Barker Vice President: Dr Khai Nguyen Secretary: Dr Peter Chen Treasurer: Dr Peter Chen State Branch Councillor: Prof Saso Ivanovski aspqld@gmail.com Meeting 1: Meeting name: Trends in Bone agents and anti-coagulants. Management and precautions Meeting date & time: 10 July pm Meeting location: Clovely Estate Cellar Door Musgrave Rd, Red Hill, QLD 4059 Speakers: Geraldine Moses Topics: Trends in Bone agents and anti-coagulants. Management and precautions Cost & other details: Free for members $140 for non-members and guests Meeting 2: Meeting name: Professor GJ Seymour and MP Cullinan Research Medallion competition Meeting date & time: 18th September - 6 pm Meeting location: Clovely Estate Cellar Door Musgrave Rd, Red Hill, QLD 4059 Speakers: Post Graduate and Honours students Topics: Research presentations by recent students with research in periodontology Cost & other details: Free for members $140 for non-members and guests Meeting 3: Meeting name: ASP Q Clinic Day The Business of Implantology Meeting date & time: 17th November Meeting location: To be confirmed Speakers: Dr. Francesco Cairo (International Speaker) Topics: The Business of Implantology The Bone, The Soft tissue and The Implant Cost & other details: Free for members $140 for non-members and guests 39

42 A VOLUME 1 Issue 1 June 2017 Australian Society of Periodontology State Branch News ASP VIC President: Dr Sarah Chin Vice President: Dr Leela Movva Secretary: Dr William Zhang Branch Councillor: Prof Ivan Darby aspvic@gmail.com Meeting 1: Meeting name: ASPVB Meeting date & time: Wednesday 29th March Meeting location: 6.00 pm Rydges on Swanston Speakers: Dr Jessica Wei Topics: The changes in periodontal microbiota in patients with hypothyroidism Cost & other details: Member: Attending both the lecturer and dinner: $80 (ASP VB) Attending lecture only: Please RSVP No Charge Non-member: Attending both the lecture and dinner: $150 Attending lecture only: Please RSVP $70 Meeting 2: Meeting name: ASPVB Meeting date & time: Wednesday 19th July Meeting location: 6:00 pm Rydges on Swanston Speakers: Drs Shayne Callis and Boris Cherkasski Topics: Synergy of Prosthodontic and Periodontic philosophies in treatment planning and management Cost & other details: Member: Attending both the lecturer and dinner: $80 (ASP VB) Attending lecture only: Please RSVP No Charge Non-member: Attending both the lecture and dinner: $150 Attending lecture only: Please RSVP $70 Meeting 3: Meeting name: ASPVB Meeting date & time: Wednesday 15th November Meeting location: 6.00 pm Rydges on Swanston Speakers: A/ Prof Axel Spahr Topics: Periodontal regeneration modern techniques, prognosis, case selection and future concepts Cost & other details: Member: Attending both the lecturer and dinner: $80 (ASP VB) Attending lecture only: Please RSVP No Charge Non-member: Attending both the lecture and dinner: $150 Attending lecture only: Please RSVP $70 40

43 VOLUME 1 Issue 1 June 2017 Australasian Osseointegration Society State Branch News A AOS NSW President: Dr Eugene Foo Secretary: Dr KY Zee Treasurer: Dr Bruce Munroe Federal Councillor: Dr George Pal Secretariat: Kayla Ashkar infonsw@aos.org.au Meeting 1: Meeting Name: Half Day Meeting Meeting Date & Time: Friday, 16 June :45 pm - 9 pm Meeting Location: Pullman Hyde Park 36 College Street, Sydney Speakers: Drs Larry Benge, Anthony Dickinson & Alex Fibishenko Topic: The Terminal Dentition - Our speakers will discuss their approach to dealing with implant treatment of the terminal dentition. Come and listen to their wealth of experience dealing with different approaches to full arch rehabilitation at our half day meeting on Friday June 16th 2017 Cost & Other Details: Visitors: $330 / Students: $275 / Complimentary for Members Membership Renewal: 1st July 2017 AOS Membership Renewal Due visit AOS website for membership details Meeting 2: Meeting Name: Dinner Meeting Meeting Date & Time: Tuesday, 19 September pm Pre-Dinner Drinks for 6:30 pm Meeting Location: TBA Speaker: Prof. Alessandro Pozzi Topic: New digital workflows in implant dentistry Cost & Other Details: See NSW branch meetings at: Meeting 3: Meeting Name: Half Day Meeting Meeting Date & Time: Thursday, 19 October :45 pm - 9 pm Meeting Location: Amora Jamison Hotel, 11 Jamison St, Sydney Speaker: Prof. Tord Berglundh Topic: Current challenges in implant dentistry. Peri-implantitis diagnosis, prevalence, risk factors and treatment Cost & Other Details: Visitors: $330 / Students: $275 / Members: $99 AOS VIC President: Dr Adam Keyes-Tilley Secretary: Dr Simon Watson Treasurer: Dr Angelos Sourial Federal Councillor: Dr Timothy Stolz Secretariat: Bella Cherkasskaya aosvic@gmail.com Meeting 1: Meeting name: AOS VB Dinner - meeting Meeting date & time: 8 June :30 pm Meeting location: Fenix 680 Victoria Street, Richmond Victoria 3121 Speakers: Professor Saso Ivanovski (Griffith University, QLD) Topics: Nature vs Nurture - genetic and environmental risk factors for biological complications 3 D Printing for bone regeneration: Challenges and opportunities Cost & other details: Members free, non-members - $190 Membership Renewal: 1st July 2017 AOS Membership Renewal Due visit AOS website for membership details 41

44 A VOLUME 1 Issue 1 June 2017 Australasian Osseointegration Society State Branch News AOS VIC (continued) Meeting 2: Meeting name: AOS VB Dinner - meeting Meeting date & time: 20 September pm Meeting location: Fenix 680 Victoria Street, Richmond Victoria 3121 Speakers: Prof Pozzi (Italy) Topics: Guided surgery Cost & other details: Members free, non-members - $190 Meeting 3: Meeting name: AOS AUSTRALIAN TOUR Meeting date & time: 21 October am 3 pm Meeting location: Fenix 680 Victoria Street, Richmond Victoria 3121 Speakers: Professor Tord Berglundh (University of Gothenburg, Sweden) Topics: Current challenges in implant dentistry. Peri-implantitis diagnosis, prevalence, risk factors and treatment Cost & other details: Members free, non-members - $ 550 Meeting 4: Meeting name: AOS 11th Biennial Conference Meeting date & time: 2-5 May 2018 Meeting location: Melbourne Convention Centre 1 Convention Centre Place, South Wharf, Victoria Speakers: Prof Tomas Albrektsson, Prof Irena Sailor, Clin Prof Frank Schwarz and Assoc Prof Stefan Fickl, more to be announced soon. Topics: Planning today for tomorrow s success Cost & other details: see website www. aosconference.com.au AOS SA President: Dr Davor Hribar Secretary: Mr Hab Awwad Treasurer: Dr Chris Hodge Federal Councillor: Dr Alan Broughton Secretariat: Francine Poole infosa@aos.org.au Meeting 1: Meeting name: AOS SA presents Professor Alessandro Pozzi Meeting date & time: Monday September 18, 2017, 6.00 pm registration Meeting location: Adelaide Intercontinental Speakers: Professor Alessandro Pozzi Topics: New digital workflows in implant dentistry Cost & other details: See SA branch meetings at: Meeting 2: Meeting name: AOS SA presents Victor Harbor weekend seminar Meeting date & time: Friday 24th November (full day) Saturday 25th November (half day) Meeting location: McCracken Country Club, Victor Harbor SA Speakers: Professor Anthony Pogrel Dr Stephen Langford Dr Vladmir Hotinski Professor Bob Jones Dr Ben Sellick Dr Elena Hotinski Dr Matthew Newman Dr Davor Hribar Topics: Essential issues that are not discussed but you should know Cost & other details: See SA branch meetings at: 42

45 VOLUME 1 Issue 1 June 2017 Australasian Osseointegration Society State Branch News A AOS QLD Acting President/Treasurer/ Federal Councillor: Dr Anthony Speed Secretary: Dr Alice Yang aosqld@gmail.com Meeting 1: Meeting name: AOS Queensland Dinner Meeting Meeting date & time: 10th May :16 pm Meeting location: Tatersalls Club Queens street Brisbane Speakers: Dr Philip Tan Topics: Digital Implant Dentistry Cost & other details: Free for members, guests are welcome register before at aosqld@gmail.com $140 Meeting 2: Meeting name: AOS Queensland Dinner Meeting Meeting date & time: 14th June :15 pm Meeting location: Tatersalls Club Queens street Brisbane Speakers: Professor Saso Ivanovski Topics: Bone Regeneration in Implant Dentistry: Current Status and Future perspectives Cost & other details: Free for members, guests are welcome register before at aosqld@gmail.com $140 Membership Renewal: 1st July 2017 AOS Membership Renewal Due visit AOS website for membership details Meeting 3 Meeting name: AOS Queensland Dinner Meeting & AGM Meeting date & time: 23rd August :15 pm Meeting location: Tatersalls Club Queens street Brisbane Speakers: Professor Pauline Ford Topics: University Of Queensland Dental School and Implant dentistry Cost & other details: Free for members, guests are welcome register before at aosqld@gmail.com $140 Meeting 4 Meeting name: AOS Queensland Dinner Meeting Meeting date & time: 12th September :15 pm Meeting location: Tatersalls Club Queens street Brisbane Speakers: Dr Carlo Maiorana (Italy) Topics: All about BioOss risks benefits when to use when to place implants Cost & other details: Free for members, guests are welcome register before at aosqld@gmail.com $145 Meeting 5 Meeting name: AOS Queensland extended meeting Meeting date & time: 17th October :00 pm - 9:00 pm Afternoon tea and dinner included Meeting location: Tatersalls Club Queens street Brisbane Speakers: Professor Tord Berglundh (Sweden) Topics: perimplantitis new research from Gothenburg University Cost & other details: Free for members, guests are welcome register before at aosqld@gmail.com $145 Meeting 1: Meeting name: AOS Queensland Dinner Meeting Meeting date & time: 6th March :15 pm Meeting location: Tatersalls Club Queens street Brisbane Speakers: Griffith University Masters student presentations Topics: To be Advised Cost & other details: Free for members, guests are welcome register before at aosqld@gmail.com $145 43

46 A VOLUME 1 Issue 1 June 2017 Australasian Osseointegration Society State Branch News AOS WA President: Dr Tony Strangio Secretary: Dr Frances Denney Treasurer: Dr Richard Williams Federal Councillor: Dr Roy Sarmidi Secretariat/Admin: Dr Frances Denny infowa@aos.org.au Meeting 1: Meeting name: AOS WA Dinner Meeting Meeting date & time: Friday, 12th May 2017 Meeting location: UWA Club Speakers: Dr. Alan Broughton Topics: Common Mechanisms of Implant Component Failure and Retrieval of Fractured Implant Component Screws Cost & other details: $110 for AOS WA members; $250 for non members Membership Renewal: 1st July 2017 AOS Membership Renewal Due visit AOS website for membership details Meeting 2: Meeting name: AOS WA AGM Dinner meeting Meeting date & time: Friday, 28th of July 2017 Meeting location: UWA Club Speakers: Dr. Vijay Tumulury Topics: The use of short dental implants and ridge preservation Cost & other details: $110 for AOS WA members; $250 for non members Meeting 3: Meeting name: AOS Australian Roadshow 2017 Meeting date & time: Monday, 23rd October 2017 Meeting location: Pan Pacific Perth Speakers: Prof. Tord Berglundh Topics: Current Challenges in Implant Dentistry and Peri-implantitis Cost & other details: $300 for AOS WA Members; $550 for non-members Find out online... Meeting details are also available online: Australian Society of Periodontology Or check with your state branch Secretary/Secretariat for further details. Australasian Osseointegration Society Or check with your state branch Secretary/Secretariat for further details. 44

47 2018 Australasian Osseointegration Society Conference 2-5 May 2018 Melbourne Convention Centre INVITATION TO ATTEND Save the Date 2-5 May 2018 Melbourne Convention Centre Melbourne INTERNATIONAL FACULTY PROGRAM AT A GLANCE IMPORTANT DATES CONFERENCE MANAGERS

48 Respects your needs. Today and tomorrow. NEW Implantmed with W&H Osstell ISQ module for reliable treatment results. Implant stability can be measured precisely with the W&H Osstell ISQ module, available as an accessory. In combination with the torque control it greatly increases the reliability of the treatment process. Upgrade at any time for today and tomorrow! Now available from your dental supplier or via wh.com Chairs Delivery Systems Lights Monitor Mounts Cabinets Handpieces Maintenance Sterilisation Imaging For more information Phone: Visit: Follow us on 2016 A-dec Inc. All rights reserved. INK _AA_ImplantMed_Bite_Oct16_1B.indd 1 30/08/ :04 am