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Dr. Peter Galgut reviews the literature on the incidence and definitions of peri-mucositis and peri-implantitis, and offers strategies for more effective diagnosis and their effective clinical management in clinical practice
Receive CE credits by taking the Galgut Quiz now.
Educational aims and objectives The aim of this article is to explore the literature on the incidence and definitions of peri-mucositis and peri-implantitis and to highlight effective clinical management of these conditions. Expected outcomes Correctly answering the questions following the article, worth 2 hours of verifiable CE, will demonstrate that the reader is able to: • Expand his/her knowledge of the published work on peri-implantitis • Explain the etiology of peri-mucositis, peri-implantitis, and periodontal diseases • Describe peri-implant inflammatory change and a diagnostic strategy for its management.
Increasing numbers of implants are being placed, and the majority of them are clinically successful. However, a significant number of failures have been reported. It is difficult to establish what percentages of implants are failing, because different authorities define failure in different ways. Most authorities consider implant failure to be a lack of osseous integration resulting in the implant being encased in fibrous tissue rather than bone. In the absence of osseous integration, implants are therefore described as having failed. However, implants that have failed to integrate, or have become mobile and require extraction, represent only one relatively minor cause of implant failure.
Increasingly, published papers are describing deteriorating peri-implant conditions that can result in loss or removal of the implant. These conditions, called peri-mucositis and peri-implantitis, are roughly equivalent to periodontal diseases that occur around natural teeth in susceptible individuals.Peri-implantitis: published workImplant failure may be the result of a number of clinical situations, such as poor restorative dentistry, premature loading, and surgical difficulties in placement. Research has indicated that failure rates of implants over a 5-year period may be as high as 37%, with as many as 80% of implants exhibiting bleeding on probing (Kent JN et al, 1990) and 54% of implants contaminated by dental plaque (Lekholm U et al, 1986; Mengel R et al, 2007).
Therefore, large numbers of implants may be failing due to a periodontitis-like condition that has been termed peri-implantitis, albeit they have not actually failed yet. Several studies have confirmed that the microbial populations around inflamed implants are similar to those found in periodontitis sites (Mombelli A et al, 1995; Eke PI et al, 1998; van Winklenhoff AJ et al, 2000).
George et al (1994) have shown that microbial pathogens associated with periodontitis occur more commonly around implants exhibiting gingival inflammation. Fardal et al (1999) have even described a case of “severe, rapidly progressing peri-implantitis” in which most of the implants were lost within 2 years of placement.
Mombelli et al (1995) have shown a higher tendency to develop peri-implantitis in patients with a known susceptibility to periodontitis.
Other experimental evidence suggests that peri-implantitis may result in significant bone loss as early as 3 months after placement due to bacterial contamination from periodontopathic organisms (Piattelli A et al, 1998).
Marinello et al (1995) demonstrated that 3 months after reversing active experimental peri-implantitis in an animal model, some sites healed by the formation of a fibrous capsule, while in other sites the inflammatory lesion continued to progress in an active destructive state in a way similar to periodontitis. They also reported that in one dog, three of the four implants were lost within 12 months, implying that some subjects may be highly susceptible to rapid and highly destructive peri-implantitis once the inflammatory process starts. This is reminiscent of the progression of the inflammatory lesion in the more aggressive forms of periodontitis.
More recently, Karoussis et al (2003; 2004) presented evidence linking periodontal and peri-implant conditions, and the incidence of peri-implant loss of attachment over a 10-year period in partially edentulous patients. They reported that in patients who were smokers and had a history of treated periodontitis, even with a 3- to 6-monthly regular recall schedule, 47.6% of implants suffered from peri-implantitis, whereas only 19.8% were affected in non-periodontitis patients.
Other studies have confirmed the existence of this condition in periodontally compromised patients (Sbordone L et al, 1999; Mengel R et al, 2001).
Eposito and Worthington (2000) performed a systematic review of health maintenance around implants, and they concluded that our knowledge of the condition and its management was inadequate. In a prior paper by this research team (Eposito M et al, 1998), the biological factors contributing to implant failure were investigated. They highlighted the multifactorial etiology of this condition, citing systemic host factors such as smoking and medically compromised patients with impaired wound healing, as well as local factors that included host factors such as poor bone density quality and anatomy, parafunctional forces, and microbial biofilm dynamics. These factors were independent of implant failure factors such as premature loading, overloading, implant design characteristics, the design of the superstructure, and operator technique.
Galgut et al (2001) have quoted percentage failure rates for implants demonstrating that those failing as a result of peri-implantitis, and/or insufficient maintenance post-placement, are much higher when the implants were placed by oral surgeons as opposed to periodontists, who presumably are more acutely aware of gingival inflammation and its consequences, as well as the subtle nuances relating to handling of the gingival tissues during, and after, surgery.
McDermott et al (2003) reported on the causative factors in long-term implant failures. These factors included smoking, single-stage implants, and surgical complications arising from anatomical defects in the bone during placement. In a study of artificially induced experimental peri-implantitis in an animal model, 1 implant out of a total of 22 was lost within 2 months of placement, while a further 2 implants were lost during the 12-month observational period following reversal of the experiment (Zitzmann NU et al, 2004). These workers also observed that 16 of the 21 remaining implants underwent further bone loss during the observational period after removal of the ligatures used to induce the inflammatory process.
In another study, a substantial sample of 677 patients observed over an 8-year period, it was reported that the overall rate of implant complications was 13.9% (McDermott NE et al, 2003). While 10.2% of complications arose from gingival inflammation, only 2.7% arose from prosthetic problems and 1.0% from operative difficulties. Therefore, current research suggests that a large number of long-term implant failures are caused by the inflammatory equivalent of periodontitis, known generally as peri-implantitis. Although implant failure is usually attributed to prosthetic complications or failures of osseous integration, a significant number of implants are failing (although they have not actually “failed” yet) due to inflammation that is associated with poor oral-hygiene maintenance and the development of peri-implantitis.
Therefore, although claims of success rates for implant placement in excess of 90% are common, these generally refer to retention of the implants in function. A large number of implants that are subject to peri-implantitis are not included in these claims. In the same way as periodontitis might progress to tooth loss, peri-implantitis may result in the loss of implants. Just as recurrent periodontal pocketing can occur around teeth of patients who have suffered periodontal destruction in the past, peri-implantitis can (and does) occur recurrently around implants in apparently healthy mouths. This is highlighted in studies by Berglund et al (carried out between 1988 and 1992), which have reported that the often-quoted ±5% failure rate may be a gross underestimation of the problem. His group reported that of the 300 implant patients in the study, 28% showed significant bone loss around implants after 10 years.
More recent work has reported that although the long-term treatment outcomes of successfully treated periodontally affected dentitions and implants show similar results (Holm-Pedersen P et al, 2007), in dentitions susceptible to recurrent periodontitis there is a marked increase in susceptibility to ongoing peri-implantitis (Mengel R, Flores-de Jacoby L, 2005; van der Weijden GA et al, 2005; Ong CT et al, 2008).
At the European workshop on periodontology held in 2008, it was reported that peri-mucositis occurred at approximately 50% of implant sites, and peri-implantitis at between 28% and 40% of sites.
Other studies have shown that peri-implant mucositis occurred in approximately 80% of subjects and in 50% of the implants. Peri-implantitis was found in 28% and 56% or more subjects and in 12% and 43% of implant sites (Zitzmann NU et al, 2004; Zitzmann NU, Berglundh T, 2008).Etiology of peri-mucositis and peri-implantitis and periodontal diseasesNumerous studies have demonstrated that a clear relationship exists between dental plaque and gingivitis, but factors beyond dental plaque are necessary to predispose individuals to periodontal diseases. Periodontitis and peri-implantitis have a multi-factoral etiology, which is summarized in Figure 1.
Environmental factors such as smoking and stress, psychological states such as depression and anxiety, and detrimental life events are all well recognized co-factors in the etiology of periodontitis and may also be factors in the etiology of peri-implantitis. Certain medical conditions, such as diabetes, are known to compromise the immune response, and therefore, increase the susceptibility of patients to periodontal/peri-implant diseases.
However, some individuals are more susceptible to periodontal breakdown due to other factors, such as genetic polymorphisms (i.e., variations in the sequence of amino acids on the DNA of chromosomes, which determine the variations in gene function). Studies into genetic polymorphisms have concentrated on the genes for coding inflammatory mediating molecules such as interleukins (IL-1, IL-6 and IL-8), prostaglandins (PG), tumor necrosis factors (TNFα) and matrix metalloproteinase (MMP)(Kornman KS, di Giovine FS, 1998; Diehl SR et al, 1999: Kobayashi T et al, 2000; Graves DT et al, 1998). Specific genotypes have identified individuals with a high susceptibility to severe periodontal destruction. It has been shown that exaggerated responses to infection attributable to genetic factors may be present in as many as one in four individuals. Interleukin 1ß has been associated with severe inflammatory responses, particularly in destructive periodontal diseases. In animal studies, inhibition of interleukin production has been shown to result in significant reductions in bone loss (Graves DT et al, 1998).
Consequently, the etiology and management of periodontal diseases (and therefore, by association, peri-implant diseases) has to concentrate not only on managing the infective condition as effectively as possible, but also the genetic background of individuals and the host responses to the infecting organisms that are directly related to the genetic factors described above (Salve GE, Lang NP, 2005).
Another major problem is the recognition that there are a number of different “periodontal diseases”! In other words, not all periodontal disease is the same. The classifications and terminology for these conditions change every few years, but currently the classification includes chronic adult periodontitis, aggressive periodontitis (which includes such conditions as early onset and refractory periodontitis), and periodontitis complicated by medical and other factors.
It is now believed that periodontal diseases are not only site-specific (in other words some sites are more susceptible than others) but also that different sites are randomly affected at different times. Also, there seem to be periods of activity and quiescence, so the condition seems to come and go and wander around the mouth haphazardly. This is known as the “random burst hypothesis” of periodontal disease progression (Goodson JM et al, 1983). It is also increasingly recognized that pockets can heal, so that pocket depths appear to reduce with time in some areas, increase in others, and yet in others don’t seem to change at all! Most importantly, peri-implantitis has increasingly been shown to have a similar etiology and pathogenesis to periodontal diseases.
Berglundh (2010) has described three risk factors for peri-implantitis:1. A life-long susceptibility to periodontal disease—just as for periodontal disease patients, at-risk implant patients require vigorous supportive therapy, with reviews four times a year and regular maintenance therapy. In some patients, implants are contraindicated due to their susceptibility to periodontal diseases2. Prosthesis design—clinicians need to ensure that anatomical, easy-to-clean restorations are placed, and that meticulous oral-hygiene maintenance is achievable by the patient, to achieve implant survival3. Implant design and surface characteristics—these are crucial prerequisites to long-term implant success. Experimental studies in dogs have shown that the progression of ligature-induced peri-implantitis is more pronounced in rough-surface implants than smooth surface. Other studies have shown that rough-surface implants demonstrate more bone surface loss in ligature-induced peri-implantitis than smooth-surface implants (Albouy JP et al, 2008; 2009).DefinitionsIt has always been thought that periodontal disease cannot occur around an implant because no periodontium exists to become inflamed. However, even relatively mild inflammation in peri-implant crevices and supporting gingival tissue cuffs may rapidly lead to inflammation spreading into the underlying tissues. As there are no periodontal fibers to become inflamed, the inflammatory process spreads directly into bone, causing a local osteitis. This condition, known as peri-implantitis, as well as other inflammatory states such as peri-implant mucositis, are clinically very similar to periodontitis and gingivitis in their presentation and pathogenesis.
The first European workshop on periodontology defined peri-implantitis as an inflammatory process affecting the tissues around an osseointegrated implant in function, resulting in loss of supporting bone (quoted in Mombelli A, Lang NP, 1998), while peri-implant mucositis has been defined as a reversible inflammatory process of the superficial soft tissues that surround implants in function.
These definitions were further defined at the sixth European workshop. Currently the definition is that “peri-implant mucositis is an inflammatory lesion that resides in the mucosa, while peri-implantitis also affects the supporting bone” (Lindhe J, Meyle J, 2008). Peri-implantitis is a generic disease in that it affects all implant systems, with no exceptions. Periodontitis and peri-implantitis have many features in common. Peri-implantitis is more aggressive and progresses faster than periodontitis, and it would appear that the implant surface does influence the disease progression.
In summary, bleeding or suppuration on probing plus bone loss equals peri-implantitis. By contrast, peri-implant mucositis is characterized by bleeding or suppuration on probing without bone loss.
It is important to define the terminology routinely used in published research on this subject but generally used ambiguously:• Failed implant—an implant that requires extraction because it is no longer osseointegrated, because it is associated with peri-implant infection or it has become irreparably damaged• Failing implant—an implant suffering progressive bone loss and therefore loss of osseous integration, associated with peri-implant infection such as peri-implantitis.Diagnosis of peri-implant inflammatory changeBerglundh (2010) described the clinical diagnosis of peri-implantitis. According to him, this is achieved using clinical and radiographic assessments of the tissues around implants in much the same way as periodontal diseases are diagnosed. He has emphasized the need for routine use of a periodontal probe to determine the presence of bleeding in the peri-implant tissues. He has also highlighted the importance of radiographs, which must be taken at prosthesis delivery (baseline) and 1 year, and then at regular intervals depending on the individual clinical circumstances. As a large percentage of implants placed in periodontitis-susceptible patients fail with time (see references above), it is crucially important to distinguish between healthy peri-implant tissues and tissues succumbing to peri-implant mucositis and/or peri-implantitis, and to intervene effectively when they are present. A diagnostic strategy for managing peri-implant inflammationThe only way of effectively diagnosing a periodontal pocket, and similarly a peri-implantitis pocket, is by use of a periodontal probe. However, the current paradigm dictates that the peri-implant tissues should not be probed for fear of damaging the delicate peri-implant cuff. The next step is to work out the best way to prevent and manage this condition before it becomes so extensive that its prognosis is all but hopeless, as shown in the case illustrated in Figures 2, 3, and 4.
The importance of meticulous clinical data cannot be overemphasized. Thus, for diagnostic purposes, the following clinical variables must be annotated in the patient’s records:1. Initial data at placement—it is imperative that a note is made of the height of the transmucosal attachment and a baseline radiograph is taken at the time of placement so that there is a record of the initial peri-implant crevice depths and bone levels.2. Discharges and bad odors—implants associated with bad odor, bad tastes, or if the patient complains of pus or other discharges, because they are clear indicators of active infection, and it is essential to bring the condition under control.3. Visual observation—assess if the gingivae are normal, pink, and healthy, or if they are edematous, red and bleeding, or discharging pus or other fluid, or otherwise abnormal. Vigorous clinical intervention is necessary if the signs are present.4. Bleeding—does the patient describe any bleeding occurring during oral-hygiene maintenance or normal function? Do the gingivae bleed during the clinical examination? Bleeding is the premier indicator of active inflammation. Any signs of bleeding should be further investigated using a periodontal probe, introducing it under the gingival margin by no more than 1.5 mm and sweeping it around the implant, following the contour of the gingival margin. If bleeding occurs, this is a positive diagnosis of active inflammatory change, which, by definition, will have resulted in contamination of the implant surface by biofilm, dental plaque bacteria, food debris, and other accretions. It is therefore perfectly justifiable to introduce a metal periodontal probe into this highly contaminated environment to determine the state of the subgingival tissues. Significant bleeding and/or discharge with or without suppuration are warning signs that active inflammation is not only present but probably converting from a superficial peri-implant mucositis to a more deep-seated and destructive peri-implantitis.5. Probing crevice depths—probing depths around implants are more difficult to assess than around teeth. It is important to compare initial crevice depths noted at the time of placement (as emphasized earlier) and the characteristics of the different constructional formats of the transmucosal attachments. This will identify variations in diameter and depth, which must be taken into account when probing into the crevices. Furthermore, as there is not a proper junctional epithelial base with supracrestal peri-implant fibers, as occurs around a natural tooth, probing should be carried out only very gently so as not to damage the delicate mucosa at the base of the crevice. Any significant increase in the depths of the crevice relative to the known depths of the transmucosal attachments recorded at baseline (also taking into account any gingival recession that may have occurred since placement) indicates that the destructive process has begun and needs to be addressed vigorously as a matter of urgency.6. Radiographs—taking pre-operative radiographs is mandatory, as is taking good-quality diagnostic radiographs immediately after placement of the implants. If there are signs of inflammation as described in the previous three paragraphs, particularly if it seems as though the conversion is taking place from superficial peri-implant mucositis to destructive peri-implantitis, follow-up radiographs need to be taken at frequent intervals thereafter, integrated with whatever maintenance or treatment and management strategy for the inflammatory condition is adopted. If the tissues look healthy, and there are no signs of bleeding, then it is wise to take another radiograph 1 year postoperatively and, in the absence of inflammatory change, annually or biannually thereafter, or at even more extended periods depending on clinical health status.
In periodontally susceptible patients, there is a high chance of peri-implantitis developing, which may lead to the loss of the implant. Therefore, any signs of destructive change need to be managed vigorously and as soon as possible, before the implant itself is compromised. With these patients, it is essential to arrange more frequent maintenance appointments and to take follow-up diagnostic radiographs at least annually, even if the superficial soft tissues are not displaying any inflammatory change.
The radiographs should be examined and compared with the baseline in order to observe any changes that may have taken place (accepting that in the first year some minor cratering in the bone is often observed at the neck of the implant after placement), as well as any exposure of the threads or increasing numbers of threads being exposed over time. This indicates peri-implantitis that will almost inevitably lead to implant failure and needs to be managed effectively.Highlighting the problems in diagnosing peri-implantitisFigures 2-4 illustrate a typical patient who has had an implant placed at the UR4. Oral hygiene maintenance is good, and the gingival tissues give the appearance of health. A slight darkening of the gingival tissues is seen around the implant. This characteristic seen around a tooth usually indicates underlying inflammation, although around an implant it may simply represent a shadow from the underlying metal of the implant.
Figure 3 is a radiograph of this implant. Excellent osseous integration seems to have occurred, but very careful examination ofthe radiograph demonstrates a slight radiolucency mesially, where there is an almost imperceptible infrabony defect, apparently only about 3 mm or 4 mm in depth. Figure 4 shows a very extensive pocket with an extensive infrabony defect present mesially that is approximately 7 mm in depth.
It is important to emphasize that neither the initial clinical appearance nor the radiographic view of the tissues in this case gave any indication that there was a major periodontal-like defect present that, sooner or later, could result in loss of the implant.
It should be noted that both in the case of implants (as illustrated in this case) and around natural teeth, the radiographic appearance of alveolar bone is notoriously inaccurate, and often underestimates or even masks the extent of infrabony defects due to the presence of buccal and/or linguo-palatal cortical plates. Therefore, radiographs are of very limited use in the diagnosis of infrabony pockets, especially around implants. ConclusionThis article demonstrates that peri-implant inflammation occurs around significant numbers of implants, particularly in patients with a history of tooth loss caused by destructive periodontal diseases. It is essential that the clinician monitor implants at regular intervals after placement for signs of inflammatory change that could convert to peri-implantitis. As with periodontal diseases, the earlier the presence of peri-implant inflammation is identified and treatment started, the greater the likelihood of arresting the condition before the destructive process compromises the retention of the implant. If inflammatory change is not identified, and the destructive process is initiated, a healthy osseous-integrated implant will inevitably convert to a failing implant and then, in time, a failed implant. It is the responsibility of the clinician to prevent this from happening.
Peter Galgut, PhD, MPhil, MSc, MRD RCS, BDS, LDS RCS, DGDP RCS, MFHom(Dent), FHEA, CUEW, is a practicing periodontist in London and a world-renowned lecturer. Dr. Galgut has published more than 100 research papers and has written a textbook on periodontics (Periodontics: Current Concepts and Treatment Strategies). He is also a qualified homeopath and acupuncturist. Dr. Galgut recently launched a website offering help and advice in the management of periodontal conditions for colleagues who do not have a local periodontist. Visit www.periodontal-diagnosis.com.
Albouy JP, Abrahamsson I, Persson LG, Berglundh T (2008) Spontaneous progression of peri-implantitis at different types of implants. An experimental study in dogs. I: clinical and radiographic observations. Clin Oral Implants Res 19(10): 997-1002.Albouy JP, Abrahamsson I, Persson LG, Berglundh T (2009) Spontaneous progression of ligatured induced peri-implantitis at implants with different surface characteristics. An experimental study in dogs. II: histological observations. Clin Oral Implants Res 20(4): 366-71.Berglundh T (2010) Peri-implantitis – characteristics, prevalence and implant surface as a risk. ADI conference: focus on peri-implantitis.Diehl SR (1999) Linkage disequilibrium of interleukin-1 genetic polymorphisms with early-onset periodontitis. J Periodontol 70: 418-430.Eke PI, Braswell LD, Fritz ME (1998) Microbiota associated with experimental peri-implantitis and periodontitis in adult Macaca mulatta monkeys. 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Periodontol 2000 17: 63-76.Ong CT et al (2008) Systematic review of implant outcomes in treated periodontitis subjects. J Clin Periodontol 35(5): 438-62.Piattelli A, Scarano A, Piattelli M (1989) Histologic observations on 230 retrieved dental implants: eight years’ experience (1989-1996). J Periodontol 69: 178-184.Salve GE, Lang NP (2005) Host response modulation in the management of periodontal diseases. J Clin Periodontol 32 (Supp 6): 108-129.Sbordone L et al (1999) Longitudinal study of dental implants in a periodontally compromised population. J Periodontol 70: 1322-1329.Van Winklenhoff AJ (2000) Early colonisation of dental implants by putative periodontal pathogens in partially edentulous patients. Clin Oral Implants Res 11: 511-520.Van der Weijden GA, van Bemmel KM, Renvert S (2005) Implant therapy in partially edentulous, periodontally compromised patients: a review. J Clin Periodontol 32(5): 506.Zitzmann NU, Berglundh T, Ericsson I, Lindhe J (2004) Spontaneous progression of experimentally induced peri-implantitis. J Clin Periodontol 31: 845-849.Zitzmann NU, Berglundh T (2008) Definition and prevalence of peri-implant diseases. J Clin Periodontol 35(8 Suppl): 286-91.
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