The Australian Journal of Periodontology and Implant Dentistry Limited The Official Journal of the Australian Society of Periodontology and the Australasian Osseointegration Society A S O www.ajpid.org.au 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 A A A S S S S S O O O Australasian ation Osseointegra ed Society limite VOLUME 1 | Issue 1 | June 2017
Transcript
The Australian Journal of Periodontology and Implant Dentistry Limited
The Offi cial Journal of the Australian Society of Periodontology and the Australasian Osseointegration Society
A SO
www.ajpid.org.au
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
Australian Journal of Periodontology and Implant Dentistry aims to promote the fi eld 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 e-mail 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, fi gures, photographs and radiographs should be submitted either contained in the Word fi le or in separately clearly labeled fi les.
References should be set out in the Uniform Requirement (Vancouver) style. Identify references in the text, tables and legends by the fi rst 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.
SubscriptionAll 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: [email protected]
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A SOEditor’s Notes
Welcome
Welcome to the fi rst 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 fi rst 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 scientifi c evidence for its use is somewhat lacking.
The second article looks at the colonisation of the oral cavity from birth by the microfl ora. 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
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A SO 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 fi rst 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 long-
standing 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 www.ajpid.org.au
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, 2018. The theme of the meeting is ‘Perio Power – how dentistry can profi t 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, www.aosconference.com.au. 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 www.aos.org.au.
We hope you enjoy this fi rst issue, and issues to come, of Australian Journal of Periodontology and Implant Dentistry.
Dr Fritz Heitz Dr Simon WatsonASP Federal President AOS Federal President
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The Effectiveness of Azithromycin in Periodontitis and Peri-implantitis
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 effi cacy 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 peri-implantitis by reviewing the clinical and microbiological parameters of the most cited studies. Although some authors have demonstrated certain benefi ts 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 microfl ora over scaling and root planing alone, particularly 12 months after administration. Peri-implant infl ammation 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
Abstract:
Gabriel Rodriguez-Ortiz
Introduction
Periodontitis is an infectious disease of the host caused by the activities of specifi c 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 biofi lm, 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 biofi lm structure they have a reduced susceptibility to antimicrobials compared to planktonic or free fl oating bacteria. Therefore, mechanical debridement is considered crucial to disrupt the biofi lm when using systemic antibiotics to treat periodontitis (Heitz-Mayfi eld, 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 biofi lms 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 infl ammation in the periodontal pocket. Herrera et al (2002), indicated that systemic antibiotics used in conjunction with scaling and root planing can offer an additional benefi t 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 fi ndings 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
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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 benefi ts 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 benefi t (Emingil, 2012; Han, 2012, Sampaio, 2011).
Azithromycin
Azithromycin is a wide-spectrum bacteriostatic macrolide with in vitro activity against aerobic and anaerobic gram-negative 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 fl uid (GCF) are higher and more sustained than in serum (Lai et al. 2011). Azithromycin is detectable in infl amed periodontal tissues >14 days after systemic administration (Gomi et al. 2007a; Gladue, 1898, 1990), allowing once-daily dosing (500 mg) for 3–6 days (Henry, 2003).
Azithromycin is found in high concentrations in fi broblasts and phagocytes (McDonald & Pruul 1991) and is carried to areas of infl ammation 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 effi cacy 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 diffi cult.
Effi cacy of Azithromycin in periodontal disease
In the fi rst 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 signifi cantly 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 signifi cance. Based in those results it is concluded by Smith et al, that the greatest benefi ts of adjunctive azithromycin therapy will be in deeper pockets. In addition, the results of this study demonstrate both statistically signifi cant and
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Author/year Type Case No Test/Cont
Intervention Follow up time
Summary Comments
Smith, 2012
R, DB, PC
23/21 T:SRP+AZMC:SRP+Placebo
0, 1, 2, 3, 6, 10, 22 weeks
PD’s initially 4–5 mm or 6–9 mm showed signi� cantly more depth reduction in patients on AZM, at weeks 6, 10 and 22.
Short study, uncertain whether controlled for smoking
Mascarenhas, 2005
R, SB 15/15 T:SRP+AZMC:SRP
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 micro� ora in AZM group
Bene� cial effect of AZM shown in smokers
Haffajee, 2007
R, SB 25/23 T:SRP+AZMC:SRP
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,
Study not controlled for smoking. Severity/diagnosis of periodontitis at baseline dif� cult to assess. Study was not placebo controlled
Oteo, 2010
R, DB, PC
15/13 T:SRP+AZMC:SRP+Placebo
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.
Small number of subjects further compromised by including both smokers and nonsmokers
Haas, 2012
RCT 12/12 T:SRP+AZMC:SRP+Placebo
Greater PD reductions, CA gain in AZM group for up to 12 mo.
Five smokers out of 24 subjects. Study not properly controlled for smoking status
Gomi, 2007
R 17/17 T:SRP+AZMC:SRP
5, 13, 25 weeks
Greater reductions in mean PD, number of bleeding on probing sites and GCF levels at 13 and 25 wk.
Short study, not properly controlled
Yashima, 2009
R, DB 10/10 T:SRP+AZMC:SRP
1, 3, 6, 9, 12 mo
Greater PD reductions, CA gain, number of BOP, GI in AZM group for up to 12 mo.
Different treatments for test and control groups make results dif� cult to compare
Dastor, 2007
RCT 15/15 T:SRP+AZMC:SRP AAll had periodontal surgery with osseous contouring after initial SRP; all subjects were given 600 mg of ibuprofen after surgery.+Placebo
Sustained reduction in periodontal pathogens in AZM group. No signi� cant difference was found for BOP, PD or CAL between both groups
Only study of effects of AZM after periodontal surgery; cannot compare with other studies
Table 1: Group of studies showing benefi ts of AZM in periodontal therapy. Modifi ed from Hirsh et al (2012)
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clinically relevant benefi ts 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 signifi cantly 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 signifi cantly 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 confi rmed 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 signifi cant shift in the bacterial ecology (Gomi et al., 2007). The long term clinical signifi cance of these fi ndings is also not clear, as it was found that, although an initial difference in bacterial profi le was present between subjects who had taken azithromycin compared to those who did not, there was no statistically signifi cant 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 confi rmed 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 signifi cant greater pocket reductions in the azithromycin and metronidazole groups, that maintained a statistically signifi cant 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 fi nding 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 benefi t 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
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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 signifi cantly 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 signifi cantly 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 diffi culty 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 signifi cantly 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 signifi cant better clinical outcome parameters, including 81% PPD reduction and 51% CAL gain of ≥2mm, compared to SRP. This was probably the fi rst study showing the clinical effi cacy 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 microfl ora 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 benefi cial 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 post- treatment. 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 signifi cant 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 specifi c clinical profi le, the mean number of sites with probing depth ≥5 mm in these subjects was much higher (approximately 60 sites)
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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 signifi cantly 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 signifi cantly 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 benefi cial change in the subgingival microbial profi le than that of azithromycin. It may be observed from this study that
scaling and root planing + metronidazole + amoxicillin was the only treatment that signifi cantly 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 benefi cial 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 benefi cial change in the microbial profi le; however, one important aspect to point out in this fi gure 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
Baseline probing depth
Variables Time period Treatment groups P*
SRP(n = 15)
SRP + AZM(n = 15)
SRP + MET + AMOX (n = 15)
4–6 mm Probing depth reduction (mm)
0–3 months 1.3 ` 0.5A 1.7 ` 0.3 1.8 ` 0.5B 0.024
0–6 months 1.5 ` 0.4A 1.6 ` 0.3 1.9 ` 0.5B 0.026
0–1 year 1.5 ` 0.5A 1.5 ` 0.4A 2.1 ` 0.4B 0.002
Clinical attachment gain (mm)
0–3 months 0.9 ` 0.3A 1.2 ` 0.3 1.4 ` 0.5B 0.002
0–6 months 1.0 ` 0.3A 1.2 ` 0.4 1.5 ` 0.4B 0.001
0–1 year 1.1 ` 0.6A 1.1 ` 0.4A 1.8 ` 0.5B 0.001
≥7 mm Probing depth reduction (mm)
0–3 months 2.5 ` 0.7A 3.4 ` 0.6B 3.9 ` 0.7B 0.000
0–6 months 2.8 ` 0.8A 3.4 ` 0.5 4.3 ` 0.8B 0.000
0–1 year 2.9 ` 0.8A 3.3 ` 0.9 4.4 ` 0.7B 0.000
Clinical attachment gain (mm)
0–3 months 1.5 ` 0.7A 2.5 ` 0.6C 3.0 ` 0.5B 0.000
0–6 months 1.8 ` 0.6A 2.5 ` 0.6C 3.4 ` 0.7B 0.000
0–1 year 2.0 ` 1.2A 2.6 ` 0.8 3.5 ` 0.6B 0.000
Values are given as mean ` SD. *The signi� cance 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 signi� cant differences between pairs of groups).
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 sub-jects 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)
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over that obtained with scaling and root planing only. These results indicate that azithromycin does not yield the same benefi ts 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 fi nding 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 signifi cant 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 fl ap 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 non-surgically, the systemic administration of azithromycin furthermore yielded signifi cant gains in overall CAL compared to baseline, whereas placebo did not.
Although it would require more research to confi rm 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 infl ammation 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 signifi cant improvements in terms of AL and PD as well as improvements in the microbiological profi le compared to baseline values. However, there was no signifi cant 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 signifi cant improvement from baseline, as well as a signifi cant difference between groups at 3 months. In terms of microbiological parameters used, there was also a signifi cant 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 effi cacy 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-infl ammatory 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 signifi cant periodontal research.
Azithromycin and Peri-implantitis
Peri-implantitis (PI) is an infl ammatory 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 biofi lm structures also appears to attach easily to titanium surfaces (Peltonen et
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al. 2007). Pseudomonas aeruginosa and Staphylococcus aureus have both been identifi ed in oral titanium related peri-implant lesions (Persson et al. 2011). In addition, studies have also shown a similarity in bacterial fl ora 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 fl ap 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 scientifi c evidence that could support this approach and none of the reports available have used a control group. Thus the clinical effi cacy 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 effi cacy 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 benefi t 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 benefi t of the adjunct use of the antimicrobial. However, this should be seen in the context of the known effi cacy of mechanical therapy alone in the treatment of perimucositis, which may be suffi cient to resolve local infl ammation (Heitz-Mayfi eld 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 benefi ts 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 benefi t.
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.
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Presents: Professor Marco Esposito
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FULL DAY SEMINARImplant dentistry, an evidence-based overview
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Colonisation of the Oral Cavity: Birth to Late Teenage Years
Fiona K. Chan
The oral cavity harbours a diverse microbiome which exists as structurally-organised biofi lms 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 biofi lm 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 identifi cation 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 identifi ed. 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.
The oral cavity harbours a diverse microbiome which exists as structurally-organised biofi lms 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 infl uence the colonization of the oral cavity and composition of the biofi lm.
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 biofi lm (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 biofi lm
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 biofi lm 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 biofi lm, initially there is formation of a conditioning fi lm 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 biofi lm via co-aggregation interactions. The sequential colonisation by other organisms and multiplication of the bacteria lead to
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an increase in the biomass. The outcome of this microbial succession leads to an increase in the complexity and thickness of the biofi lm over time. Finally, an equilibrium state or climax community is reached where there is a balance between biofi lm growth and loss of bacteria into the environment (Marsh & Bradshaw, 1995). As the biofi lm 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 biofi lm can become pathogenic if environmental perturbations triggers a catastrophic shift in the balance of the resident microfl ora (Marsh & Bradshaw, 1995). In 1998, Socransky et al. proposed that the microfl ora 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 identifi ed 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).
Infl uences on colonisation of the oral cavity
Host response The host immune system can infl uence the colonising ability of microbes in the oral cavity. Infants are particularly susceptible to microbial colonization as their immune systems are immature and specifi c 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 specifi cally 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 microfl ora of preterm neonates requiring prolonged hospital care and normal neonates (Rotimi & Duerden, 1981).
Whilst it is clear that the composition of the oral fl ora can be infl uenced by changes in the environment, host genetics has also been proposed as an infl uencing factor on bacterial colonization. Moore et al. examined twin children living in the same households and found that the subgingival microfl ora of identical twins were more similar than those of fraternal twins, indicating that there may be some genetic control over the composition of the microfl ora (Moore et al., 1993).
Bacterial virulence factors Virulence factors can infl uence 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
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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 signifi cant 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 microfl ora in infants include pacifi ers, 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 infl uenced by host, microbial and environmental factors. Whilst it is recognised that the biofi lm is dynamic and the microbial profi le 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 fi rst 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 identifi ed 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 identifi ed 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-specifi c 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
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(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 fi rst 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 fi ndings 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 fi rst 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 biofi lm formation (Bradshaw et al., 1998). Among the ‘late colonizers’, the prevalence of Capnocytophaga spp. increased to 10% towards the end of the fi rst 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 microfl ora in the oral environment increases with the eruption of teeth (Carlsson, Grahnén, & Jonsson, 1975; Pearce et al., 1995; Rotimi & Duerden, 1981). After the fi rst 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 biofi lms on oral surfaces also offer a more favourable microenvironment for the colonisation of anaerobes (Costerton et al., 1994).
During the fi rst 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 signifi cant levels. In the early mixed and mixed dentition stage, C. showae, a member of the orange complex, increased signifi cantly 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.
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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 fi ndings 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 fi rst 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 fi ndings 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 fl ora differed signifi cantly 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 fi ndings 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 infl uence 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 microfl ora 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 pre-pubertal 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 infl amed sites compared with non-infl amed 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).
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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 Classifi cation 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 early-onset periodontitis patients (Vandesteen et al., 1984; Williams et al., 1985). Specifi cally, 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 signifi cantly 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 biofi lm 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 signifi cantly 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 microfl ora, it should be recognised that the colonisation of the oral cavity is also infl uenced 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 diffi culties in processing large numbers of samples and challenges in the collection of microbial samples from
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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 profi le differs markedly on the various intraoral surfaces (Tanner et al., 2002). As such, the microbiota collected from one location may not fully refl ect 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 identifi cation 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 signifi cant 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 infl uence 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 biofi lm 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 identifi cation of potential causative agents of periodontal disease allows for a greater understanding of the overall disease process, as yet, no single cause has been identifi ed. 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
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Dental Implant Screw Mechanics
Louis Kei, Iven Klineberg
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 scientifi c literature on implant screw mechanics.
Method: A search of the English language peer-reviewed 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 identifi ed 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 misfi t, functional forces, implant diameter, number of implants, passive fi t of prosthesis, torque wrench, repeated opening and closing of the screws, and splinting versus non-splinting 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.
The use of implant-supported single crowns and implant-supported fi xed 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 fi xture 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 fi xture and holds the fi xture 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 specifi c torque for each screw/abutment assembly of which is dictated by the material and design of the specifi c 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
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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
PreloadMcGlumphy 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 signifi cant 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 signifi cant 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 coatingThe material of which the abutment or prosthetic screw is fabricated from directly infl uences 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 coeffi cient 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)
• TiCN coating(9)• TiN coating(3)• Parylene N coating(9)• Tefl on 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
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used for fi xation. 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 Tefl on 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 specifi c preload data of the new coated-screws prior to its use.
Screw designJorneus et al compared the preload generated by 2 abutment screw head designs (fl at head and conical head) and found a signifi cantly 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 fi xed 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 diffi cult to apply manual force when tightening a slotted screw because of the clinician’s anxiety concerning driver slippage from the slot.
Abutment / Implant interface misfi tThe abutment / implant interface misfi t has been considered a signifi cant 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 fi xture – a proxy for abutment/implant interface misfi t, 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 misfi t between internal and external hexagons ranged from 1.94 degrees for the smallest abutment to 14.87 degrees for the largest. It was found there was a strong direct correlation between the amount of hexagonal misfi t and screw loosening. The authors concluded the greater the rotational freedom, the greater the probability of screw loosening.
Abutment / Implant interface designThe 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 well-designed A/I interface can signifi cantly 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 fi xture and subjected the implant-abutment assembly to simulated functional loading. It was found the absence of the external implant hex extension signifi cantly 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 fi xture), 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 forcesMcGlumphy and colleagues proposed the following strategies to minimize joint separating forces to the implant abutment assembly(2):
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Bakaeen et al investigated infl uence 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 signifi cant 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 implantBoggan and colleagues conducted a laboratory study on the infl uence of implant platform diameter on the mechanical strength and quality of fi t of the implant-abutment 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 implantsBakaeen 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 16660 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 fi t of prosthesisIn a retrospective study by Kallus and Bessing, patients restored with implant-retained and -supported fi xed dental prostheses were more likely to have gold prosthetic screw loosening when their prosthesis was judged to have a misfi t between the framework and the abutments by a calibrated examiner(10).
Torque wrenchThe 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 closingDuring impression and prosthesis fabrication, repeated closing and opening of abutment screws may cause component wear and decrease frictional fi t 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 fi rst 30 openings. The authors concluded that the reduction in opening torque was probably due to a decrease in the coeffi cient 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 fi rst 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).
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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 implantsClelland 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 fi xed 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:
Screw selection 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 con� rms 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)
Screw tightening 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
Abutment / Implant connection selection
Use reputable implant manufacturers to ensure high quality and precisely machined A/I � t
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)
Prosthesis design Minimise cantelever
Ensure passive framework � t
Splint adjacent implants
Implant selection Use a wide platform implant in posterior regions
Use 2x regular neck implants to replace a large molar if possible
Occlusal design Minimise excursive contacts
Minimise off-axis centric contacts
Reduce cusp height and angles
Reduce width of occlusal table
Torque wrench Annual calibration to ensure accurate torque output of the torque wrench
Inspection for any corrosion in the spring component in detent joint wrenches
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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 head2. Retrieve the crown along with the abutment3. Once the crown and abutment were removed, a
radiograph was taken to reconfi rm the fractured part of the abutment screw inside the implant
4. A fi ne 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 fl ame-shaped bur is modifi ed to prepare a groove
on the fractured screw. The diamond particles of the upper part of the fl ame-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 piece3. 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.
References1. Albrektsson T, Donos N, Working G. Implant survival and complications. The Third EAO consensus conference 2012. Clinical oral implants research. 2012;23 Suppl 6:63-5.
2. McGlumphy EA, Mendel DA, Holloway JA. Implant Screw Mechanics. Dent Clin N Am. 1998;42:71-89.
3. 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):24-32.
4. Haack JE, Sakaguchi RL, Sun T, Coffey JP. Elongation and preload stress in dental implant abutment screws. Int J Oral Maxillofac Implants. 1995;10:529-36.
5. Winkler S, Ring K, Ring JD, Boberick KG. Implant screw mechanics and the settling effect: An overview. J Oral Implantol. 2003;29:242-5.
6. 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;7:353-9.
7. Siamos G, Winkler S, Boberick KG. The relationship between implant preload and screw loosening on implant-supported prostheses. J Oral Implantol. 2002;28:67-73.
8. 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;15:164-71.
9. Elias CN, Figueira DC, Rios PR. Infl uence of the coating material on the loosing of dental implant abutment screw joints. Materials Science and Engineering. 2006;26:1361-6.
10. Kallus T, Bessing C. Loose gold screws frequently occur in full-arch fi xed prostheses supported by osseointegrated implants after 5 years. Int J Oral Maxillofac Implants. 1994;9:169-78.
11. Binon PP. Evaluation of machining accuracy and consistency of selected implants, standard abutments, and laboratory analogs. Int J Prosthodont. 1995;8:162-78.
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12. Binon PP. The effect of implant/abutment hexagonal misfi t on screw joint stability. Int J Prosthodont. 1996;9:149-60.
13. 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):326-34.
14. Weiss EI, Kozak D, Gross MD. Effect of repeated closures on opening torque values in seven abutment-implant systems. J Prosthet Dent. 2000;84:194-9.
15. 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;27:63-72.
16. Boggan RS, Strong JT, Misch CE, Bidez MW. Infl uence of hex geometry and prosthetic table width on static and fatigue strength of dental implants. J Prosthet Dent. 1999;82(4):436-40.
17. Gutierrez J, Nicholls JI, Libman WJ, Butson TJ. Accuracy of the implant torque wrench following time in clinical service. Int J Prosthodont. 1997;17:562-7.
18. 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;88:183-91.
19. 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):1135-41.
20. 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):747-50.
21. Kurt M, Guler AU, Duran I. A technique for removal of a fractured implant abutment screw. J Oral Implantol. 2013;39(6):723-5.
Professor Tord Berglundh, Sweden.DDS, PhD Professor Department of Periodontology Institute of Odontology
Sahlgrenska Academy University of Gothenburg.
Proudly sponsored by
CURRENT CHALLENGES IN IMPLANT DENTISTRY. PERI-IMPLANTITIS - DIAGNOSIS, PREVALENCE,
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
For details, pricing and registration please check the website www.aos.org.au
AOS PRESENTS HALF-DAY EVENT
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Australian Periodontology Research Foundation Report 2017
The APRF continues to enjoy and benefi t 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-implantitisInstitute: University of MelbourneInvestigators: 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 trialInstitute: University of Western AustraliaInvestigators: 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 studyInstitute: 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 studyInstitute: University of SydneyInvestigators: S Madukuri, A Spahr, J Mahon, F Zahr
Th17 cells in chronic periodontal diseaseInstitute: University of MelbourneInvestigators: 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 SydneyInvestigators: J Vo, A Spahr
The effect of azithromycin on the treatment of peri-implant infectionInstitute: University of SydneyInvestigators: L Gershenfeld, S Yeung, A Spahr
The effect of azithromycin on the treatment of peri-implant infectionInstitute: University of SydneyInvestigators: A Kalos, S Yeung
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Platinum Level - $10,000 per annumColgate Oral Care
Titanium Level - $3,000 per annumDentsply ImplantsNobel Biocare
Website
The APRF now has an online presence as part of the ASP website at http://www.asp.asn.au/Information on the APRF is available for download.
Silver Level - $2,000 per annumStraumann
Bronze Level - $1,000 per annumHenry Schein Halas
An evaluation of whole biofi lm models on titanium implants: a proof of concept studyInstitute: University of QueenslandInvestigators: C Tran, L Walsh
Effi cacy of azithromycin compared with other antibiotics used in the clinical practice for the treatment of Aggregatibacter actinomycetemcomitans associated periodontal diseaseInstitution: University of MelbourneInvestigators: 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 Griffi th University for the paper “The effect of platelet proteins released in response to titanium implant surfaces on macrophage pro-infl ammatory cytokine gene expression. Clin Implant Dent Relat Res 2015 Dec;17(6):1036-47.” 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:
Meeting Date & Time: Friday, 16 June 2017 – 3:45 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 www.aos.org.au for membership details
Meeting 2:
Meeting Name: Dinner Meeting
Meeting Date & Time: Tuesday, 19 September 2017 – 6 pm Pre-Dinner Drinks for 6:30 pm
Meeting Location: TBA
Speaker: Prof. Alessandro Pozzi
Topic: New digital workfl ows in implant dentistry
Cost & Other Details: See NSW branch meetings at: www.aos.org.au
Meeting 3:
Meeting Name: Half Day Meeting
Meeting Date & Time: Thursday, 19 October 2017 – 3:45 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”
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 workfl ows in implant dentistry
Cost & other details: See SA branch meetings at: www.aos.org.au
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 PogrelDr Stephen LangfordDr Vladmir HotinskiProfessor Bob JonesDr Ben SellickDr Elena HotinskiDr Matthew NewmanDr Davor Hribar
Topics: Essential issues that are not discussed but you should know
Cost & other details: See SA branch meetings at: www.aos.org.au
AOS SA
Australasian Osseointegration Society State Branch News
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Acting President/Treasurer/ Federal Councillor: Dr Anthony Speed
Industry Sponsor Closing PlenaryKeynote Presentaons
1500 - 1830 Registraon Open
1715 - 1830Industry Recepon
1900 - 2130 Welcome Recepon
1900 - 2400Conference Gala Dinner
* Preliminary program subject to change
ICMS Pty Ltd Suite 2, 191 Riversdale Road PO Box 170Hawthorn VIC 3122Phone: 1300 792 466Email: [email protected]
CONFERENCE MANAGERS
www.aosconference.com.au
Call for Abstracts OpenJune 2017
Call for Abstracts Closes1 December 2017
Early Bird Registraon Closes26 January 2018
IMP
OR
TAN
TD
ATES
INVITATION TO ATTEND
Dear Colleagues, On behalf of the Federal execuve and the organising commi�ees of the Australasian Osseointegraon Society, it is with much pleasure that I invite you to a�end our 11th Biennial Conference, to be held in Melbourne from the 3rd - 5th May 2018.
The meeng is a mechanism for dental clinicians, academic researchers and industry partners to come together to promote dental implant treatment modalies, evaluate emerging research, technology and techniques, and share new ideas, in order to improve current procedural techniques for all.
Planning is well underway for a full 3-day program to smulate the interests of a wide range of clinicians' experience, and our industry sponsors and partners will be pu�ng together an excellent trade display where you can meet and discuss the latest developments in materials and instrumentaon for successful clinical pracce. Our speakers will include academic researchers and expert clinicians, with highly regarded internaonal speakers and invited local speakers who are experts in their respecve fields coming to speak on a variety of topics including treatment planning, surgery, restoraon and maintenance.
Of course there will be a number of social events to mix with colleagues including a welcoming drinks event and a grand dinner. Being based in the Southbank area of Melbourne, there are many restaurants and bars for catching up with friends, industry representaves and other colleagues.
We hope you can join us in May, 2018. Simon WatsonDCD (Prosthodoncs), BDScFederal President of the Australasian Osseointegraon Society.
2018Australasian Osseointegration Society Conference2-5 May 2018
Melbourne Convention Centre
www.aosconference.com.au
Tomas Albrektsson MD PhD OdhcProfessor Emeritus, Department of Biomaterials, Instute of Clinical Sciences, Gothenburg, Sweden
Lyndon Cooper DDS, PhDAssociate Dean for Research, Head of the Department of Oral Biology , The University of Illinois at Chicago, College of Denstry
Stefan Fickl DMD, PhDAssociate Professor, Department of P e r i o d o n c s , U n i v e r s i t y o f Wuerzburg, Germany
Irena Sailer Prof. Dr. med. dent. Prof. and Chair, Division of Fixed Prosthodoncs and Biomaterials, Clinic of Dental Medicine, University of Geneva, Switzerland
Frank Schwarz Clinical Professor, Heinrich Heine University, Düsseldorf, Germany
INTERNATIONAL FACULTY
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2-5 May 2018
Melbourne Convention Centre
Melbourne
For more information Email: [email protected] Phone: 1800 225 010 Visit: www.wh.com Follow us on Twitter: @A_decAust
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