Key Systemic and Environmental Risk Factors for Implant Failure

Dental implants are an important treatment option for patients interested in replacing lost or missing teeth. Although a robust body of literature has reviewed risk factors for tooth loss, the evidence for risk factors associated with dental implants is less well defined. This article focuses on key systemic risk factors relating to dental implant failure, as well as on perimucositis and peri-implantitis.

Key points

  • Dental implant failure is related to several risk factors, including systemic disease, periodontal disease, and environmental factors.

  • Poorly controlled disease may contribute to perimucositis and peri-implantitis, potentially leading to implant complications, including failure.

  • Although few risk factors are absolute contraindications to implant placement, further research is needed to determine which combination(s) of factors predisposes patients to perimucositis and peri-implantitis, important precursors to implant failure.


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.


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.


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


A substantial amount of literature has examined the relationship between diabetes and periodontitis. A number of these studies have supported a bidirectional relationship in which improving the overall status of one disease may improve the status of the other. The hyperglycemic state of diabetes, if left unchecked, results in shifts in the advanced glycation end product/receptor for AGE (AGE/RAGE) axis and the receptor activator of nuclear factor-κB ligand and osteoprotegerin (RANKL/OPG) axis and can lead to overall immune and cytokine imbalance, as well as cellular stress. This imbalance can contribute to periodontal pathogenesis by enhancing tissue destruction and can also result in impaired healing. There seems to be a dose-dependent relationship between severity of periodontitis and diabetes, and evidence indicates that periodontitis control can improve diabetes control. Likewise, patients with poorly controlled diabetes tend to have an increased likelihood of and severity of periodontal disease.

As with periodontal therapy, it is believed that good control of diabetes (hemoglobin A1c ≤ 7) can contribute to successful implant therapy. A review by Bornstein and colleagues found that the rate of implant failure was higher among diabetic patients and that these patients experienced earlier implant failure than patients without diabetes. Given the importance of controlling periodontal inflammation relative to diabetes, it may be worthwhile to consider the relationship between peri-implant tissues and diabetes. Several animal studies have examined osseointegration in terms of bone quality or timing of failure, as well as other clinical parameters. A study using a diabetes-induced pig model found that diabetic pigs had less bone-to-implant contact than nondiabetic pigs. Rats injected with AGEs exhibited a slower rate of osseointegration, and the injections had a negative effect on implant stability. Another study using diabetic rats found decreased bone density around osseointegrated implants. A study followed several clinical parameters over a period of 3 years in patients with various levels of diabetic control as measured by hemoglobin A1c levels. Within the 4 levels of diabetic control defined by the study, the highest level (hemoglobin A1c ≥ 10.1) was associated with the greatest level of bleeding on probing and a greater bleeding level over the course of 3 years. On the other hand, a recent review of glycemic control and implant therapy failed to find a relationship between levels of glycemic control and implant failure.

Although some studies have investigated the level of inflammatory cytokines relative to diabetes and periodontitis, there is a paucity of information about inflammatory biomarkers in the perimucosal tissues of diabetic patients. An animal model using rates with type 2 diabetes to study proinflammatory markers and growth factors related to healing of bone after implant placement found delayed osteoblast differentiation and decreased levels of IL-1β, tumor necrosis factor (TNF)-α, and macrophages. A study by Venza and colleagues evaluated proinflammatory gene expression in patients with or without diabetes and found that levels of TNF-α, CCR5, and CXR3 were higher in sites with peri-implantitis ( P <.01) in patients without diabetes or with well-controlled diabetes. The levels of TNF-α, CCR5, and CXR3 were higher in chronic periodontitis sites in poorly controlled diabetics. Further work is needed to clarify the proinflammatory and anti-inflammatory responses in peri-implant tissues in diabetic patients.


A number of reviews indicate positive correlations between obesity or hyperlipidemia and periodontitis, particularly as it relates to metabolic syndrome. Currently, there is a lack of information about how hyperlipidemia may affect the risk of implant failure or peri-implant inflammation.

Impaired Organ Function

The number of published studies reporting the risk of implant failure associated with impaired organ function is limited. Studies focused on the success of implants in patients who have received organ transplants (ie, heart, liver) have found that the clinical parameters and radiographs of dental implants for those patients do not differ from those of healthy patients. Because these studies have involved patients who are immunocompromised because of organ transplant, further studies are needed to determine failing organs contribute to the risk of implant failure or peri-implantitis.


Osteoporosis results in a decrease in bone density and has been considered a relative contraindication to implant placement. A significant number of more recent studies have focused on the treatment of osteoporosis with bisphosphonates, a topic that is reviewed elsewhere in this article. Recent reviews have indicated that there is no absolute contraindication to implants in patients with osteoporosis. A retrospective study of 3224 implants placed in 746 women 50 years of age or older evaluated bone mineral densities on a subset of 192 women with 646 implants with a diagnosis of either osteoporosis, osteopenia or no osteoporosis or osteopenia and found that a neither a diagnosis of osteoporosis nor osteopenia conferred a greater risk of implant failure. In this study, the risk of implant failure was 2.6 times higher for smokers than for nonsmokers.

Hormonal Disturbances

A recent review by Fu and colleagues reported the influence of glucocorticosteroids, nonsteroidal anti-inflammatory drugs, and statins on implant healing. In general, nonsteroidal anti-inflammatory drugs had a deleterious effect on bone-to-implant contact and bone density after implant placement, whereas statins seemed to have a positive effect on bone formation. Several animal studies investigating the local application of growth hormones have found a positive effect on bone formation and a loss of bone density when estrogen levels are low. A study by Moy and colleagues found that women aged 60 to 79 had a higher rate of implant failure than those 40 or younger. In this study, however, women on postmenopausal estrogen therapy had an increased risk of 2.55 times that of those postmenopausal women not on hormone replacement therapy.


Aside from bisphosphonates, no specific medication seems to be directly associated with implant failure in humans. A study investigating implants in medically treated hypothyroid patients found more bone loss and a less favorable soft tissue response after stage one surgery 1 year after implant placement but no increased risk of failure. In an animal study, the administration of cyclosporine to rabbits was associated with negative bone quantity as determined by subtractive radiography. Further studies are needed to delineate the direct effects of medications on the risk of implant failure and on peri-implant tissues.


Many patients commonly take bisphosphonates for the treatment of osteoporosis or during cancer therapy. Osteonecrosis of the jaws has been listed as a complication that may occur in some patients treated with bisphosphonates. Bisphosphonate-related osteonecrosis of the jaws (BRONJ), also called bisphosphonate-induced osteonecrosis of the jaws, can occur in patients taking an oral or intravenous bisphosphonate. Dentoalveolar trauma, such as dental extraction, seems to trigger BRONJ. The placement of dental implants in patients undergoing bisphosphonate therapy requires careful evaluation. The effect of bisphosphonates on the osseointegration of dental implants is unclear. Shabestari’s group placed 46 ITI implants in 21 osteoporotic female patients taking oral bisphosphonates. No implant mobility was recorded, and no cases of peri-implantitis were found by examination at the end of the study period. There was no effect of implant location, type of prosthesis, opposing dentition, or the time at which implant therapy began on successful osseointegration. A study by Zahid and colleagues involved 227 patients and recorded surgical complications, number of exposed implant threads, implant failure, age, gender, smoking status, systemic conditions, and medications. Of 51 implants placed in 26 patients taking bisphosphonates, 3 failed, for a success rate of 94%. No variable other than bisphosphonate therapy was associated with either implant failure or thread exposure.

Animal studies have been used to gain information difficult to obtain from human subjects. Abtahi and associates placed titanium implants in rats being treated with systemic bisphosphonates and also placed implants coated with bisphosphonates in rats not taking systemic bisphosphonates. Changes similar to those seen in osteonecrosis of the jaw were evident in the systemically treated rats, but no such changes were seen in the rats with coated implants, except for an increase in implant removal torque. Shibutani’s group used ligatures to induce peri-implantitis in 10 beagle dogs. Induction began 6 months after implant placement. A bisphosphonate (pamidronate) was injected into 5 of the dogs every 3 days for 12 weeks after the ligatures were placed. Bone loss was significantly greater in the control dogs than in dogs treated with pamidronate.

Kumar and Honne evaluated published studies that compared implant survival in users and nonusers of bisphosphonates. Five articles met their inclusion criteria. Only 1 article stated that implant failure was higher for patients taking bisphosphonates. The range of survival rates for dental implants was approximately equal for short-term users and nonusers of bisphosphonate. Lazarovici and colleagues followed 145 patients with BRONJ, 27 of whom developed BRONJ associated with dental implants. The mean time to the development of BRONJ was 16.2 months for patients who had been taking bisphosphonate therapy before implant placement.

Although much has been discovered about the effects of bisphosphonates, considerably more research is necessary for providing a clear picture for practitioners. Some studies have shown no effects, whereas others have shown both positive and negative effects. A complicating factor is time. A number of studies have found a significant time lag between implant placement and evidence of alterations in osseous structure. Until more answers are forthcoming, great care and caution would be prudent when dentists are considering the placement of implant fixtures in patients taking bisphosphonates.


Radiation therapy is often prescribed for the treatment of head and neck cancer. Adverse effects can include xerostomia and altered function of the irradiated area. A recent systematic review of irradiation and dental implants by Chambrone and colleagues evaluated the number and percentage of implants lost, with the exclusion of implants placed only in grafted areas. The risk of implant loss was 174% higher for implants placed in irradiated bone than for those placed in nonirradiated bone. The risk of loss of maxillary implants was 496% higher than the risk of loss of mandibular implants. The authors found no indication that hyperbaric oxygen therapy affected implant loss.

A retrospective study evaluated the survival of 225 implants in 30 patients who received irradiation therapy and found a 5-year success rate of 92.6%. A dose–response relationship has been observed between increases in implant failure and high-dose irradiation; some authors recommend 55 Gy as a cutoff for high-dose therapy. Others have noted continued implant loss over a long period of time after irradiation, up to 25 years in 1 study. Another study by Buddula and colleagues found that the success rates for implants placed in irradiated patients decreased over time (98.9% at 1 year, 89.9% at 5 years, and 72.3% at 10 years) and that the success rate for maxillary implants are lower than those for mandibular implants.


Genetic polymorphisms have been studied to assess their potential role in predisposition to implant failure or peri-implantitis. A number of the genes investigated parallel those that have been evaluated for periodontitis and focus on inflammation and bone turnover. A recent study examined IL-1β and TNF-α genotyping and to placement of titanium implants and reported that implant loss was significantly related to increasing number of risk genotypes of Il-1β and TNF-α. An examination of IL-1 gene clusters by Vaz and colleagues in 155 Portuguese patients with 100 successful implants and 55 unsuccessful implants (defined by the authors as “implant loss or mobility, pain on palpation, percussion or function; recurrent infection [fistula or suppuration], perimucositis, peri-implantitis, and vestibular metal exposing during or after the abutment connection”). They concluded that successful implants were associated with a negative genetic test and that unsuccessful implants were associated with a positive genetic test. An earlier review by Huynh-Ba and colleagues examined 44 studies, 2 of which were longitudinal; the authors did not find enough evidence to support or refute the contribution of the IL-1geneotype to implant failure and did not support systematic genetic testing. Casado and colleagues examined susceptibility to IL-6 G174 C and peri-implant disease in a Brazilian population and found that, at a minimum, the IL-6 genotype was 1.53 times more likely to convey peri-implant disease if the individuals had the GC genotype and allele G. Another recent study by Pigossi and colleagues examined 3 single nucleotide polymorphisms for IL-10 and found no association with implant failure.

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Oct 28, 2016 | Posted by in General Dentistry | Comments Off on Key Systemic and Environmental Risk Factors for Implant Failure

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