Key points

Introduction

Many studies have demonstrated the long-term success of dental implants in replacing teeth missing because of caries or periodontal disease. A significant number of published articles detail the success of various types of implants placed in specific situations, such as those placed in bone-augmented sites. Implant failure has long been understood as the complete loss of the dental implant, but it is becoming apparent that an increasing number of implants are associated with perimucositis or peri-implantitis. Published reports indicate that peri-implantitis affects approximately 10% of implants and 20% of patients ; however, the incidence is higher in some reports, depending on the thresholds used to define the condition. Despite the variability in definitions and the wide array of designs of the studies assessing the success or failure of implants, it is reasonable to assume that we will continue to see an increase in the prevalence of inflammatory processes that affect implants and that may lead to destruction of connective tissue or bone. This article reviews key systemic, periodontal, and environmental risk factors associated with implant failure, as well as perimucositis and peri-implantitis.

Introduction

Many studies have demonstrated the long-term success of dental implants in replacing teeth missing because of caries or periodontal disease. A significant number of published articles detail the success of various types of implants placed in specific situations, such as those placed in bone-augmented sites. Implant failure has long been understood as the complete loss of the dental implant, but it is becoming apparent that an increasing number of implants are associated with perimucositis or peri-implantitis. Published reports indicate that peri-implantitis affects approximately 10% of implants and 20% of patients ; however, the incidence is higher in some reports, depending on the thresholds used to define the condition. Despite the variability in definitions and the wide array of designs of the studies assessing the success or failure of implants, it is reasonable to assume that we will continue to see an increase in the prevalence of inflammatory processes that affect implants and that may lead to destruction of connective tissue or bone. This article reviews key systemic, periodontal, and environmental risk factors associated with implant failure, as well as perimucositis and peri-implantitis.

Microbiology of peri-implantitis and perimucositis and comparison with periodontitis

The primary etiologic factor for peri-implant mucositis is the oral biofilm. This initial challenge to the host defense mirrors the challenge that affects the natural dentition. The initial adherence of bacteria to the implant surface can vary with the type of surface topography. Implants with rough surfaces enhance the initial bacterial colonization. In general, sites affected by periodontitis and peri-implantitis contain more gram-negative bacteria than healthy sites. The types of bacteria associated with healthy implants and failing implants are similar to those associated with healthy and diseased teeth, but there are also some important differences. Kumar and colleagues used 16S pyrosequencing to analyze subgingival and submucosal plaque samples from subjects with healthy implants and from subjects with periodontitis and peri-implantitis. They found that peri-implant biofilms differed between the 2 groups: There was less diversity in the type of bacteria, but, with increasing disease, the numbers of Prevotella and Leptotrichia were lower and the numbers of Campylobacter, Actinomyces, and Peptococcus were higher. Cortelli and colleagues found that the frequency of Porphymonas gingivalis was higher in cases of peri-implantitis than in cases of perimucositis and that the levels of P gingivalis and Aggregatibacter actinomycetemcomitans were similar in periodontitis and peri-implantitis. The levels of Campylobacter rectus and Tannerella forsythia were higher in healthy gingiva than in gingiva affected by peri-implant mucositis. On the other hand, a study by Koyanagi and colleagues found more bacterial diversity in peri-implantitis sites than in periodontitis sites (198 taxa in peri-implantitis, 148 taxa in periodontitis). Fusiform bacterium and Streptococcus species were common in association with both peri-implantitis and periodontitis, whereas Parvimonas micra were seen only in association with peri-implantitis. Dabdoub and colleagues conducted a patient-specific analysis of peri-implant and periodontal microbiomes associated with implants adjacent to teeth and found significant differences in both the populations and the levels of participant microbes, concluding that the proximity of an implant to a tooth does not account for the bacterial species seen in peri-implant tissues.

The microbial community may have shared attributes and, as discussed, some differences when both natural dentition and implants are present, but what are the microbial characteristics of implants when no natural teeth are present? A study by Kocar and colleagues evaluated partially edentulous patients and found the frequency of 4 of the periodontopathogens assessed ( P gingivalis , T forsythia , T denticola , and A actinomycetemcomitans) was higher in pockets 4 mm or deeper than in shallow pockets (≤4 mm), but was not different from the frequency of these pathogens in association with implants adjacent to natural teeth. However, none of these bacteria were found in the implant sites of completely edentulous patients. Additional studies are needed to assess the progression of peri-implantitis and the microbial ecology in edentulous patients.

Reported risk factors for perimucositis and peri-implantitis include a history of previous periodontal disease. Presumably, if the periodontopathogens that exist in the peri-implant pocket are similar to those that exist in the natural dentition, then the host response and the subsequent soft tissue and hard tissue destruction would be similar to those for a natural tooth. In comparing the various levels of severity of periodontitis, Aloufi and colleagues found that the rate of loss of clinical attachment around implants was higher when severe periodontitis was present. Another study compared patients with or without residual periodontal pockets 6 mm or deeper and found that for patients with these pockets the prevalence of probing pockets 5 mm or deeper, bleeding on probing, and bone loss was higher than for patients with no residual periodontal pockets. The authors surmised that the maintenance of periodontal health is more important than a past history of periodontitis and is a crucial determinant of the risk of peri-implantitis. The result of a recent retrospective study of treatment outcomes of peri-implantitis supported the importance of maintaining periodontal health: The effectiveness of peri-implant therapy by various surgical methods was lower in association with a diagnosis of generalized or localized severe periodontitis. Other studies have also suggested that the development of peri-implantitis or the loss of implants is more likely for patients in whom reinfections of treated periodontal sites occur during maintenance therapy than for patients with periodontal stablity.

Although a number of studies have focused on the relationship between microbial ecology and the pockets associated with perimucositis or peri-implantitis, fewer studies have investigated the significance of adjacent periapical infections. Lefever and colleagues conducted a retrospective analysis of implants adjacent to teeth with endodontic pathology and found that the likelihood of the development of periapical lesions was 7.2 times higher for an implant placed next to a tooth that already has such a lesion than for an implant placed next to teeth without periapical lesions. The most prominent species found in these lesions was P gingivalis.

Smoking

The list of risk or potential risk factors for peri-implantitis or implant failure is extensive. It includes systemic disease, genetic traits, chronic drug or alcohol consumption, smoking, periodontal disease, radiotherapy, diabetes, osteoporosis, dental plaque, and poor oral hygiene. Smoking and its relationship to periodontitis has received a great deal of attention in the periodontal literature. It is well known that patients who smoke have more periodontal destruction than nonsmokers. According to the result of a study by Karbach and colleagues, smoking was also the most important risk factor for the formation of peri-implant mucositis. As the number of dental implant placements continues to increase and patients’ requests for implants become more commonplace, many dentists wonder whether their placement in smokers presents any risks for unsuccessful restoration of the dentition.

The accuracy of implant placement is crucial to implant success, especially when the alveolar ridge is narrow. D’haese and De Bruyn found small deviations between the planned location and the actual placement site of implants for smokers, but not for nonsmokers. The authors speculated that, because mucosal tissues are thicker in smokers than in nonsmokers, there was a decrease in the stability of the surgical guide or the scanning prosthesis, and that this instability caused alterations in the final placement of implants.

Many edentulous patients seek implant placement to allow the construction of a stable mandibular denture. One study compared 36 patients treated with 2 implants and ball attachments, 37 patients treated with 2 implants and a bar, and 37 patients treated with 4 implants and a triple bar attachment in the mandibular arch. The mean evaluation time for this group of patients was 8.3 years. The group with 4 implants lost significantly more bone than the groups with 2 implants. Marginal bone loss in smokers was almost twice that observed in nonsmokers, irrespective of the treatment modality. Smoking may affect the implants anchoring a fixed dental prosthesis. Wahlström and colleagues used clinical and radiographic examinations to study fixed dental prostheses in 46 patients. All fixed dental prostheses had been in function for at least 3 years. The authors found that smokers had fewer teeth, more periodontal pockets 4 mm or deeper, and a greater tendency toward increased marginal bone loss than nonsmokers. Increases in the loss of osseous support could lead to increases in implant failure and the loss of anchorage for a removable or fixed prosthesis.

The location of implants in the oral cavity may influence the overall success rate of these implants if a variation in bone loss is present. A comparison of the maxillary arches of smokers and nonsmokers showed that smokers lost slightly more than twice as much bone, whereas smokers and nonsmokers lost approximately the same amount of bone around mandibular implants. A radiographic evaluation of maxillary implants by Haas and his group showed that smokers experienced more bone resorption than nonsmokers. The analysis revealed no difference between smokers and nonsmokers in bone loss in the mandibular arch.

Kourtis and colleagues also found that the rate of implant failure was higher for smokers than for nonsmokers. They speculated that the higher failure rate may have been owing to smokers’ reduced healing capability.

A wide choice of implant surfaces is available to the practitioner, and the selection of the proper surface may make a difference in the overall failure rate. Sayardoust’s group compared turned and oxidized implants 5 years after placement in smokers and never smokers. Smokers with turned implants lost almost twice as much bone as never smokers with turned implants, whereas the failure rate for oxidized implants was almost equal for smokers and never smokers. Aalam and Nowzari compared (1) surfaces roughened by anodic oxidation (TiUnite dental implants), (2) dual acid-etched surfaces (Osseotite dental implants), and (3) machined implants (Brånemark dental implants). Smoking had no impact on the success rates of these 3 implant types. Balshe and coworkers found no significant failure rate for smokers with rough surface implants, whereas the failure rate was significant for smokers with smooth surface implants. In this study, the largest number of failures was associated with smooth surface implants placed in the posterior maxilla. In a meta-analysis, Strietzel and his associates found that the enhanced risk of implant failure was higher for smokers than for nonsmokers. Their systematic review found that the risk of biologic complications was greater in smokers than in nonsmokers. The authors found 5 published studies that reported no impact of surface types on implant prognosis, but these studies investigated only implants with particle-blasted, acid-etched, or anodic oxidized surfaces. The characteristics of implants may affect their survival rate. Surface characteristics combined with length, width, and support of a fixed prosthesis may produce differing responses in the surrounding bone. A study of 339 implants placed over a 21-year period found that annual bone loss was higher in association with implants that were shorter or wider, that supported a fixed prosthesis, or that were placed in smokers. Smokers had almost 3 times more annual bone loss than nonsmokers. The most important factor to consider for maintaining implants was implant length: Better results were achieved with longer implants.

Smoking may influence the healing of tissues after implant placement. D’Avila and associates studied the surfaces of implants placed 2 months earlier in the posterior maxilla (type IV bone) of smokers. Their histometric evaluation showed that bone-to-implant contact was twice as high for sandblasted, acid-etched implants than for machined implants. Many patients require only a single implant between 2 natural teeth.

One study performed clinical and radiographic evaluation of implants placed between 2 natural teeth at least 5 years earlier in former smokers, smokers, and nonsmokers. Although the authors concluded that smoking was not related to the rate of implant survival, current smokers experienced more marginal bone loss than former smokers or nonsmokers, and nonsmokers lost less marginal bone than any other group. Leonhardt and colleagues used surgery and antimicrobial therapy to treat peri-implantitis and followed these patients for 5 years after treatment. They concluded that treatment outcome was less favorable for smokers with severe peri-implantitis than for nonsmokers. Orthodontists use miniscrews to assist them in achieving patient treatment goals. Anything that has a negative effect on miniscrew anchorage would be detrimental to treatment outcome. Bayat and Bauss considered patients’ daily amount of smoking, defining light smokers as those who smoked fewer than 10 cigarettes per day and heavy smokers as those who smoked more than 10 cigarettes per day. The failure rate of miniscrews was higher for heavy smokers than for either light smokers or nonsmokers. The authors found no differences in miniscrew failures between light smokers and nonsmokers.

Patients testing positive for the interleukin (IL)-1 genotype have been found to be more susceptible to periodontal disease. Jansson and colleagues evaluated Brånemark implants that had been placed over a 10-year period. IL-1–positive patients in general were not more prone to implant failure, but failure rates were higher for smokers who IL-1 positive. Gruica and associates found that 64 of the 180 patients in their study were IL-1 positive. There was no significant correlation between the nonsmoking IL-1–positive patients and implant complications. However, the rates of complications and implant failures were higher in IL-1–positive smokers.

Dental practitioners always promote the practice of good oral hygiene in their practices. Oral hygiene may be a factor in increasing the success rate of implants placed in smokers. One study evaluated fixed implant-supported prosthetics in the mandibular arches of 45 patients over a 10-year period. They found good results for both smokers and nonsmokers. Marginal bone loss was higher for smokers than for nonsmokers and was even higher for smokers with poor oral hygiene.

Because many research articles have reported smoking’s negative impact on dental implants, should practitioners recommend implants for patients who smoke? A literature review by Takamiya and colleagues found that even though many negative factors were associated with smoking and dental implants, smoking was not an absolute contraindication to implant placement. The authors noted that smokers should be advised that their risk of implant failure is greater than that for nonsmokers. Heinikainen and associates sent 10 cases with various characteristics to 400 general practitioners and 47 dental teachers in Finland. They were asked if they would or would not recommend implants for each case. Approximately 50% of general practitioners but only 15% of dental teachers replied that they would recommend implants for smoking patients.

Smoking cessation therapy could be a positive factor in implant therapy. Yilmazel Ucar and colleagues used varenicline, bupropion, and nicotine replacement therapy in a smoking cessation clinic. The highest success rate was 52.8% in the nicotine replacement group. The overall success rate was 35% and the overall relapse rate was 21.6%. Yasin’s group uses behavioral therapy and free nicotine replacement to treat 185 smokers for 8 weeks. Six months after therapy, only 15% of the patients were still not smoking.

Research results show that the decision to place implants in smokers may not be clear cut. Ideally, it would be better for smokers to enter a smoking cessation program and to quit smoking before implant placement. Smoking has a negative impact on implant survival for patients with machined-surface implants, fixed prosthetics, marginal bone loss, bone-to-implant contact area, and IL-1 genotype. There is lack of agreement among dentists about whether implants should be recommended to their patients who smoke. Smoking cessation programs seem to be the ideal solution, but study results are not encouraging. Dentists who consider the use of implants for smokers must clearly explain the increased risk of implant failure to every patient.

Systemic risk factors