Implant loss is the most serious complication of dental implants. Although the problems and causes behind the implant failure are clearly defined today, determination of the underlying causes of failure varies by the case. The clusterization phenomenon of implant loss (multiple implant failures) implies the existence of genetic risk factors. Inflammation has a critical effect on osseointegration and implant success. Peri-implantitis is an inflammatory disease of tissue supporting the tooth or implant. Inflammation leads to loss of support tissue, particularly bone, resulting in failure of implants. A single nucleotide polymorphism (SNP) of pro-inflammatory mediator genes may affect their expression levels or amino acid sequence, and, consequently, the host inflammatory response. Since the end of the past century, many studies have been conducted to investigate the association of SNP with implant failure and related conditions. Involvement of several groups of genes—including interleukins, tumor necrosis factor-α, matrix metalloproteinases, and growth factors involved in immune regulation, inflammatory response, and bone metabolism—has been explored. Some have been found to be associated with implant loss and considered potential genetic risk factors for implant failure. In this review, we summarize results of recent studies of impact of genetic factors on dental implant failure.

Dental implants are widely used for the effective and predictable treatment of tooth loss. According to Albrektsson's and Karoussis's criteria, success rates of implants have reached 92.6% and 83.0%, respectively.1  The 10-year survival rate of successful implants is over 93%.1,2  Implant loss is a serious complication, categorized either as early or late loss. Early implant failure reflects only a failure in osseointegration,3  that is, loss within 6 months of implantation or before the implants are loaded.4,5  The majority of failures are due to early loss and are associated with surgical trauma, infection, and inadequate bone quantity or quality. Late loss of osseointegrated implants is categorised as that occurring beyond 6 months post-implantation.4,5  Late loss may result from mechanical damage to the implant or from biological causes leading to peri-implantitis and lack of support by surrounding bone.

Peri-implantitis and periodontitis are inflammatory and infectious diseases that result in the destruction of the tissue supporting the tooth or implant, leading to tooth/implant loss.6  Approximately 30% of patients with dental implants develop peri-implantitis.7  In addition to microbial infection, the host response plays an important role in the pathogenesis of periodontitis and peri-implantitis. Host response to microorganisms triggers the release of pro-inflammatory mediators. In physiological situations, the periodontal or peri-implant tissues in close contact with the dental biofilm have an active immune response and low-grade inflammation.6  Once the production of inflammatory mediators is dysregulated, the host cells release toxic products, resulting in tissue destruction around teeth and oral implants.6,8  Interleukin-1 (IL-1), IL-6, IL-17, and tumor necrosis factor (TNF)-α are known as strong pro-inflammatory molecules.6  The implants have also been shown to stimulate macrophages to release pro-inflammatory cytokines, such as IL-1 and TNF-α, which mediate the inflammatory and osteolytic process of peri-implantitis as well as promote the matrix metalloproteinases-mediated degradation of extracellular matrix components. However, this phenomenon happens only in a minority of patients, suggesting an important role of host factors, particularly the immune response to the implants.9  An adequate immunologic response and an appropriate tissue repair mechanism are required for implant osseointegration. So, short term or low level of inflammation with moderate IL-1 and TNF-α release benefits dental implant osseointegration. Strong or long term IL-1 and TNF-α release-mediated inflammatory and osteolytic processes enhance the risk for severe peri-implantitis and implant failure.9  In addition to bacterial plaque and host immune response, prosthetic and surgical factors can also induce peri-implantitis,10,11  suggesting that iatrogenic factors are involved in the pathogenesis of the peri-implantitis. Many iatrogenic factors, including excess cement remnants or/and incorrect finishing line, bio-corrosion, failed bone reconstruction, overloading, inappropriate restoration design, implant malpositioning, microleakage at the implant-abutment interface, abutment unscrewing, and implant crack or fracture, may be associated with peri-implantitis.1015 

Multiple factors—including implant material properties, surgical procedure, and host characteristics—affect implant success rate, and the precipitating cause of failure cannot always be identified. Early studies revealed the existence of clustering of implant failure, 1618  with multiple early losses occurring in a single individual, suggesting that genetic aspects and/or an immune response may be contributing factors.4  Inflammation has a critical effect on osseointegration and implant success. Inflammatory cytokine production induces peri-implantitis and stimulates bone resorption, resulting in implant failure. It has been reported that inflammatory mediators such as IL-1β, TNF-α, IL-8, and macrophage inflammatory protein-1α are significantly higher in the peri-implant crevicular fluid (PICF) of patients with peri-implantitis, implying that cytokines could be prognostic markers of implant failure.7,19 

A single nucleotide polymorphism (SNP) is single nucleotide variation at a specific position of the genome. Each variation appears in some appreciable degree within a population. SNP may occur within coding and non-coding sequences of genes, or in the intergenic regions. Considering degeneracy of the genetic code, SNP within a coding sequence may change the amino acid sequence of the coding polypeptide (nonsynonymous SNP), or not affect the protein sequence (synonymous SNP). SNP outside protein-coding regions may still regulate gene expression through affecting the transcription factor binding, gene splicing, mRNA degradation, or the sequence of noncoding RNA. Therefore, SNP underlies differences in our susceptibility to disease. SNP of inflammatory cytokine genes may affect their expression levels or amino acid sequence and, consequently, the host inflammatory response. The groups of genes involved in the regulation of inflammatory responses and bone metabolism have been investigated and associated, to some extent, with peri-implantitis and implant loss (Table, Figure). Based on a PubMed search using the keywords dental (oral) implants, failure (loss), and genetics (polymorphisms), this review summarizes research and updates information on the association of polymorphisms of several relevant genes with dental implant failure.

Table

Key information for studies of gene polymorphisms and implant loss*

Key information for studies of gene polymorphisms and implant loss*
Key information for studies of gene polymorphisms and implant loss*
Figure

Polymorphic sites evaluated for their association with implant loss or related disease. (-), no association; (+), association; (+/-), association or no association.

Figure

Polymorphic sites evaluated for their association with implant loss or related disease. (-), no association; (+), association; (+/-), association or no association.

Close modal

IL-1

Interleukins (IL) are a group of cytokines that play important roles in the immune response. IL-1 is a potent pro-inflammatory cytokine that maintains periodontal homeostasis and plays an essential role in pathogenesis of periodontitis.39  The functional polymorphism in the IL-1 gene may be a genetic risk factor for implant failure. Studies of IL-1 polymorphism and dental implant failure initially involved the role of IL-1 in the development of periodontitis and peri-implantitis. An early study identified the IL-1 genotype as a strong indicator of susceptibility to severe periodontitis.40  When IL-1A-889 C/T (rs1800587), IL-1A+4845 G/T (rs17561), and IL-1B+3954 C/T (rs1143634, formerly IL-1B+3953) polymorphisms were investigated, the discrepant results were achieved.22,4143  The available evidence was insufficient to confirm or refute their association with peri-implantiti.44,45  Biochemical markers of the peri-implant immune response in PICF demonstrated that the influence of IL-1A-889 C/T and IL-1B+3954 C/T on the peri-implant crevicular immune response and peri-implantitis was limited.46  The IL-1 receptor antagonist (IL-1RA) is an anti-inflammatory cytokine that binds to and blocks the IL-1 receptor and inhibits IL-1-mediated signals. Polymorphism of the IL-1RA encoding gene IL-1RN was genotyped and found that IL-1RN allele 2 was associated with peri-implantitis.47  The frequency of the IL-1RN 2/2 genotype in chronic periodontitis patients and controls was reported to be 30% and 15%, respectively.43  Data suggest that IL-1RN gene polymorphism is associated with peri-implantitis and chronic periodontitis, constituting a risk factor.43,47 

A further question is whether IL-1 polymorphisms are associated with loss of bone surrounding the implant. Polymorphisms of IL-1A-889 C/T, IL-1B-511 C/T, and IL-1B+3954 C/T were detected and a significantly higher occurrence of marginal bone loss was observed in patients with the IL-1B-511 C/T 2/2 genotype, suggesting an association of this genotype with early marginal bone loss around endosseous implants.4850  Investigation of the association of IL-1 polymorphisms in IL-1A+4845 G/T and IL-1B+3954 C/T loci with peri-implant bone loss at osseointegrated dental implants revealed that smoking and IL-1 polymorphisms were associated with an increased risk for peri-implant bone loss in osseointegrated dental implants.51 

In the past two decades, scientists have investigated the relationship between the IL-1 genotype and implant failure. An initial study found that IL-1 polymorphism did not increase the risk of implant failure, but smoking was a significant risk factor.20  Further study found no association of four polymorphisms in the IL-1 gene cluster with early failure of osseointegrated implants.2123  When the effects of IL-1A-889 C/T, IL-1A+4845 G/T, and IL-1B+3954 C/T polymorphisms and smoking on the prognosis of osseointegrated implants were evaluated, the IL-1 genotype alone did not predict implant loss, but a significant synergistic effect was found between smoking and a specific IL-1 genotype, leading to significantly higher implant loss.24,25 

The significance of IL-1 polymorphism in implant loss is a topic of debate. Polymorphisms of IL-1B+3954 C/T and IL-1RN (intron 2), both shown to alter coding protein expression, were investigated in subjects with implant loss, and genotype 2/2 of IL-1RN was significantly more frequent in individuals presenting multiple implant losses, suggesting a potential genetic basis for the clusterization phenomenon.26  Polymorphisms of IL-1A-889 C/T and IL-1B+3954 C/T were significantly associated with the status of the dental implants.27  When polymorphisms of IL-1A-889 C/T, IL-1B+3954 C/T, IL-1RN+2018 T/C (rs419598), and TNF-α-308 G/A (rs1800629) were genotyped in subjects with titanium implant failure, the minor alleles of the studied polymorphisms in the implant failure group were more frequent than in controls. The incidence of implant loss increased along with the increase in number of risk genotypes, demonstrating an additive effect.9  TNF-α and IL-1β secretion upon titanium stimulation was significantly higher in patients with implant loss.9  Data indicate that IL-1β/TNF-α release and number of risk genotypes are significantly and independently associated with titanium implant failure.9  The T allele of IL-1A-889 C/T and IL-1B+3954 C/T was significantly associated with early implant failure and the IL-1B+3954 C/T polymorphism is likely to impact osseointegration.3  A meta-analysis supported that the IL-1A-889 C/T and IL-1B+3954 C/T composite genotype and the T allele of IL-1B-511 C/T were associated with increased incidence of implant failure/loss.39 

IL-2 and IL-6

In addition to IL-1, interleukins including IL-2, IL-4, IL-6, IL-10, and IL-17 have been investigated for their association with early implant failure. IL-2 and IL-6 are cytokines involved in T-cell activation and B-cell differentiation. Both have been implicated in stimulation of osteoclast activity and bone resorption.52,53  Several studies have reported polymorphisms of IL-2-330 T/G (rs2069762),54  IL-6-174 G/C (rs1800795),5557  IL-6-1363 G/T (rs2069827), and IL-6-1480C/G57,58  to be associated with periodontitis, and G allele of polymorphism rs2069837 (A/G) located in intron 2 of IL-6, was shown to be a potential marker of protection against chronic periodontitis.59  Polymorphism of IL-2-330 T/G and IL-6-174 G/C in promoter regions contributes to the transcription activity of these cytokines. In an early study, the allele and genotype distribution of IL-2-330 T/G and IL-6-174 G/C was not significantly associated with early failure of dental implants.28  But the A Allele of IL-6 rs2069843 (A/G) and T allele of IL6+4272 C/T (rs2069849) were found to be associated with the loss of mini-implants for orthodontic anchorage.30 

IL-4

IL-4 induces differentiation of naive helper T cells and stimulates proliferation of activated B and T cells. Initial study indicated that IL-4-590 C/T (rs2243250) was not associated with severe periodontitis.60  When polymorphisms of IL-4-590 C/T, IL-4+33 C/T (rs2070874), and IL-4 70 bp variable number tandem repeat (VNTR) (rs79071878) were investigated, the alleles/genotypes of IL-4-590 C/T and IL-4 VNTR polymorphisms were not found associated with implant loss.29  Although frequency of genotype IL-4+33 C/T was not significantly different between groups, the C allele was associated with dental implant loss.29 

IL-10

IL-10 is an anti-inflammatory cytokine. Polymorphisms of IL-10-1082 A/G (rs1800896), IL-10-819 C/T (rs1800871), and IL-10-592 A/C (rs1800872) on the promoter region of the IL-10 gene have been reported to be associated with IL-10 production and autoimmune disease. When these three polymorphisms were analyzed, no allele, genotype, or haplotype was significantly associated with dental implant loss or chronic periodontitis.4,31  A study further confirmed that IL-10-1082 A/G polymorphism was not associated with failure of dental implants.32  However, polymorphism of IL-10-819 C/T and IL-10-592 A/C were associated with susceptibility to chronic periodontitis.61  When 23 candidate genes for periodontitis were evaluated, association of IL-10 rs61815643 with aggressive periodontitis was observed.62 

IL-17

IL-17 is a pro-inflammatory cytokine secreted by activated T cells.63  The IL-17 concentration was higher in tissue adjacent to degraded bone, and increased IL-17 levels have been associated with chronic periodontitis.64,65  IL-17 gene polymorphism was investigated in patients with chronic periodontitis, patients with peri-implantitis, and healthy individuals. The frequency of the CC genotype of IL-17 rs10484879 (A/C) in the peri-implantitis group was significantly higher than in healthy individuals and those with chronic periodontitis, suggesting that the CC genotype may contribute to the pathogenesis of peri-implantitis.63 

TNF-α

Tumor necrosis factor-α (TNF-α) is a pro-inflammatory mediator involved in the regulation of bone resorption.66,67  Several studies suggested that the TNF-α-308 G/A polymorphism was not associated with peri-implantitis, peri-implant bone loss, or early implant failure.31,37,68,69  In recent studies, the A allele in TNF-α-308 G/A increased the level of this cytokine and was associated with periodontitis.70,71  The AG genotype of TNF-α-308 G/A was associated with a fivefold risk of peri-implantitis compared to other genotypes.72  However, a meta-analysis concluded that TNF-α-308 G/A polymorphism was not significantly associated with the risk of peri-implant disease.73 

RANKL

Receptor activator of nuclear factor kappa B ligand (RANKL)—also known as TNF-related activation-induced cytokine or osteoprotegerin (OPG) ligand—is a member of the TNF superfamily. The RANK-RANKL-OPG signaling pathway is involved in osteoclastogenesis, osteoclast activation, and regulation of bone resorption. Polymorphisms of RANK genes rs3018362 (A/G) and rs35211496 (C/T) were investigated in individuals with peri-implantitis, with chronic periodontitis, and periodontally healthy. The CC genotype of the rs35211496 RANK gene was significantly associated with peri-implantitis and was suggested as a genetic risk factor.74  When the RANKL gene polymorphisms of rs9533156 (T/C) and RANKL+290 A/G (rs2277438) were analyzed, the CT genotype of rs9533156 was significantly associated with peri-implantitis.75  RANKL-438 A/G polymorphism was not associated with the failure of dental implants.32 

Matrix metalloproteinases (MMP) are a class of zinc-dependent proteolytic enzymes responsible for extracellular matrix metabolism that are possibly involved in the osseointegration process of dental implants.76,77  Matrix metalloproteinases have been found in peri-implant sulcular fluid, playing a pathologic role in peri-implant bone loss.78,79  The polymorphisms in MMP-1,33,34  MMP-8,75  and MMP-933 have been investigated. Polymorphisms of MMP-1-1607 G/GG (rs1799750) and MMP-1-519 A/G (rs1144393) in the promoter region of human MMP-1 have been shown to increase transcription activity.34  Polymorphism of MMP-1-1607 G/GG was reported to be associated with severe chronic periodontitis.80  The 2G allele and 2G/2G genotype in patients with severe periodontitis were significantly more frequent than in the healthy group.80  The genetic association of MMPs with periodontitis risk has been well-reviewed.81 

Polymorphism of MMP-1-1607 G/GG has been demonstrated to be associated with early implant failure.33  The frequency of the G allele and the G/G genotype in the MMP-1-1607 G/GG were 62% and 34%, respectively, in patients with one or more early failed implants, compared with 75% and 62% in control group, indicating an association with early implant failure.34  The MMP-1-519 A/G polymorphism was not significantly associated with implant loss.34  When the MMP-8-799 C/T (rs11225395) polymorphism in the promoter region of the MMP-8 gene in nonsmoking patients was investigated, it was found that the T allele and the T/T genotype were associated with early loss of implants.35  The MMP-9-1562 C/T (rs34016235) polymorphism in the MMP-9 promoter region was not associated with chronic periodontitis82  or implant loss.33 

BMP and FGF

Bone morphogenetic proteins (BMP) represent a family of growth factors that facilitate osteogenesis. The BMP-4 genetic polymorphism was found to influence marginal bone loss around implants before implant loading.83  When 13 polymorphic sites in BMP-4, FGF3, FGF10, and FGFR1 genes were analyzed, the TT genotype of BMP-4 rs2761884 (G/T) contributed to healthy peri-implant, while BMP-4 GAAA and GGGA haplotypes were associated with peri-implantitis.84  Fibroblast growth factors (FGF) and their receptors (FGFR) are involved in the regulation of cell proliferation, differentiation, and migration. The TT+CT genotypes of FGF3 rs4631909 (C/T) were more frequent in healthy controls. The C allele frequency of the FGF3 rs4631909 (C/T) and FGF10 CCTG haplotype were positively associated with peri-implantitis.84  The BMP-4 and FGF10 haplotypes showed a relationship with peri-implantitis. Bone morphogenetic protein/retinoic acid inducible neural-specific protein 3 (BRINP3) is involved in cell proliferation, migration, and death.85  Polymorphisms of BRINP3 rs1935881 (A/G) and rs1342913 (A/G) have been associated with periodontitis86  and peri-implantitis.87 

TGF-β1

Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine involved in pathophysiological functions such as reduction of inflammation and promotion of wound healing. The polymorphisms of TGF-β1-509 C/T (rs1800469) and TGF-β1-800 G/A (rs1800468) in the promoter region increase its transcription activity. Polymorphism in TGF-β1-509 C/T is likely to be associated with severe periodontitis,88  but the polymorphisms of TGF-β1-509 C/T and TGF-β1-800 G/A were not significantly associated with early implant failure.36 

Other Genes

Other genes that modulate inflammatory responses or bone metabolism have been investigated with respect to association with dental implant loss or peri-implantitis. Cluster of differentiation 14 (CD14) is involved in the immune response by acting as a co-receptor of Toll-like receptor 4 and MD-2 for the detection of bacterial lipopolysaccharide. Individuals with CC genotype of CD14-159 C/T (rs2569190) showed a fivefold risk for peri-implantitis and higher RANKL level and the RANKL/OPG ratio in peri-implant crevicular fluid.72  Polymorphisms of Toll-like receptor 289 and Toll-like receptor 490 were not associated with periodontitis. Calcitonin receptor (CTR) is involved in maintenance of calcium homeostasis and bone metabolism. Individuals with the TC genotype for CTR were 20 times more likely to suffer early marginal bone loss in the mandible than patients with the CC genotype.91  Vitamin D receptor polymorphism (rs731236) was suggested as a marker for susceptibility to chronic periodontitis92  but was not associated with dental implant loss.38  A group of small noncoding RNAs, known as miRNAs, are involved in multiple physiopathological processes. miR-146a (rs2910146) and miR-499 (rs3746444) gene polymorphisms were related to increased risk of chronic periodontitis and peri-implantitis.93  Several other genes, including PF4/PPBP/CXCL5,94  SIGLEC5, DEFA1A3,95  IFI16, AIM2,96  FBXO38, AP3B2,97  and IFIH198 have also been associated with periodontitis. The circadian rhythm system and cartilage extracellular matrix have been demonstrated to contribute to osseointegration via vitamin D regulation and influenced the success of dental implants.99  Genes encoding BRAF,100  lactotransferrin,101  and haptoglobin102  have been investigated but not found to be associated with implant loss, peri-implantitis, or periodontitis.

Dental implant loss in some patients cannot be explained by clinical factors alone, 103  and several phenomena imply the existence of genetic risk factors for implant failure.104  Implant failure does not occur randomly among populations, but multiple implant failures may occur in a single individual, demonstrating a clusterization phenomenon.17  Recurrence of implant failure is common.105  The possibility of a genetic predisposition for dental implant complications has attracted attention in the past two decades.106  Currently available data appear to support the existence of genetic susceptibility, but this remains unresolved. Discrepancies in results maybe attribute to small sample sizes and the potential limitations of data gathered from specific geographic populations. Most importantly, studies are dependent on polymorphism analysis and lack experimental evidence. Further study, with larger sample sizes in various ethnicities, is necessary to determine the effect of genetic polymorphisms. In addition, since only genes involved in immune regulation and bone metabolism have been investigated thus far, a genome-wide screen or omics-study—such as genomics, transcriptomics, proteomics, and metabolomics—will be valuable to detect genuine susceptibility genes. Finally, and critically, it is necessary to develop an animal model to carry out experimental studies to elucidate the roles and mechanisms of genetic factors. The results will be helpful for the identification of proper candidates for dental implants in clinical practice.

Abbreviations

    Abbreviations
     
  • BMP

    bone morphogenetic protein

  •  
  • BRINP3

    bone morphogenetic protein/retinoic acid inducible neural-specific protein 3

  •  
  • CD14

    cluster of differentiation 14

  •  
  • CTR

    calcitonin receptor

  •  
  • FGF

    fibroblast growth factor

  •  
  • FGFR

    fibroblast growth factor receptor

  •  
  • IL

    interleukin

  •  
  • IL-1RA

    IL-1 receptor antagonist

  •  
  • MMP

    matrix metalloproteinase

  •  
  • OPG

    osteoprotegerin

  •  
  • PICF

    peri-implant crevicular fluid

  •  
  • RANKL

    receptor activator of nuclear factor kappa B ligand

  •  
  • SNP

    single nucleotide polymorphism

  •  
  • TGF-β1

    transforming growth factor-β1

  •  
  • TNF-α

    tumor necrosis factor-α

  •  
  • VDR

    vitamin D receptor

  •  
  • VNTR

    variable number tandem repeat

This study was funded by Open Fund of Guangdong Key Laboratory of Pharmaceutical Functional Genes (No. 2014B030301028 and No. 2017B030314021).

No conflict of interest is declared.

1
Mertens
C,
Steveling
HG,
Stucke
K,
Pretzl
B,
Meyer-Baumer
A.
Fixed implant-retained rehabilitation of the edentulous maxilla: 11-year results of a prospective study
.
Clin Implant Dent Relat Res
.
2012
;
14
:
816
827
.
2
Pjetursson
BE,
Thoma
D,
Jung
R,
Zwahlen
M,
Zembic
A.
A systematic review of the survival and complication rates of implant-supported fixed dental prostheses (FDPs) after a mean observation period of at least 5 years
.
Clin Oral Implants Res
.
2012
;
23
(
suppl 6
):
22
38
.
3
Cosyn
J,
Christiaens
V,
Koningsveld
V,
et al.
An exploratory case-control study on the impact of IL-1 gene polymorphisms on early implant failure
.
Clin Implant Dent Relat Res
.
2016
;
18
:
234
240
.
4
Pigossi
SC,
Alvim-Pereira
F,
Montes
CC,
et al.
Genetic association study between Interleukin 10 gene and dental implant loss
.
Arch Oral Biol
.
2012
;
57
:
1256
1263
.
5
Shemtov-Yona
K,
Rittel
D.
On the mechanical integrity of retrieved dental implants
.
J Mech Behav Biomed Mater
.
2015
;
49
:
290
299
.
6
Frederic
LJ,
Michel
B,
Selena
T.
Oral microbes, biofilms and their role in periodontal and peri-implant diseases
.
Materials (Basel)
.
2018
;
11
:
1802
.
7
Schminke
B,
Vom Orde F, Gruber R, Schliephake H, Burgers R, Miosge N. The pathology of bone tissue during peri-implantitis
.
J Dent Res
.
2015
;
94
:
354
361
.
8
Wong
HC,
Ooi
Y,
Pulikkotil
SJ,
Naing
C.
The role of three interleukin 10 gene polymorphisms (−1082 A > G, −819 C > T, −592 A > C) in the risk of chronic and aggressive periodontitis: a meta-analysis and trial sequential analysis
.
BMC Oral Health
.
2018
;
18
:
171
.
9
Jacobi-Gresser
E,
Huesker
K,
Schutt
S.
Genetic and immunological markers predict titanium implant failure: a retrospective study
.
Int J Oral Maxillofac Surg
.
2013
;
42
:
537
543
.
10
Canullo
L,
Tallarico
M,
Radovanovic
S,
Delibasic
B,
Covani
U,
Rakic
M.
Distinguishing predictive profiles for patient-based risk assessment and diagnostics of plaque induced, surgically and prosthetically triggered peri-implantitis
.
Clin Oral Implants Res
.
2016
;
27
:
1243
1250
.
11
Canullo
L,
Schlee
M,
Wagner
W,
Covani
U.
Peri-implant
MGS:
International brainstorming meeting on etiologic and risk factors of peri-implantitis, Montegrotto (Padua, Italy), August 2014
.
Int J Oral Max Impl
.
2015
;
30
:
1093
1104
.
12
Linkevicius
T,
Puisys
A,
Vindasiute
E,
Linkeviciene
L,
Apse
P.
Does residual cement around implant-supported restorations cause peri-implant disease? A retrospective case analysis
.
Clin Oral Implants Res
.
2013
;
24
:
1179
1184
.
13
Pesce
P,
Canullo
L,
Grusovin
MG,
de Bruyn
H,
Cosyn
J,
Pera
P:
Systematic review of some prosthetic risk factors for periimplantitis
.
J Prosthet Dent
.
2015
;
114
:
346
350
.
14
Alani
A,
Bishop
K.
Peri-implantitis. Part 2: prevention and maintenance of peri-implant health
.
Br Dent J
.
2014
;
217
:
289
297
.
15
Sasada
Y,
Cochran
DL.
Implant-abutment connections: a review of biologic consequences and peri-implantitis implications
.
Int J Oral Maxillofac Implants
.
2017
;
32
:
1296
1307
.
16
Weyant
RJ,
Burt
BA.
An assessment of survival rates and within-patient clustering of failures for endosseous oral implants
.
J Dent Res
.
1993
;
72
:
2
8
.
17
Tonetti
MS.
Determination of the success and failure of root-form osseointegrated dental implants
.
Adv Dent Res
.
1999
;
13
:
173
180
.
18
Fransson
C,
Lekholm
U,
Jemt
T,
Berglundh
T.
Prevalence of subjects with progressive bone loss at implants
.
Clin Oral Implan Res
.
2005
;
16
:
440
446
.
19
Petkovic
AB,
Matic
SM,
Stamatovic
NV,
et al.
Proinflammatory cytokines (IL-1beta and TNF-alpha) and chemokines (IL-8 and MIP-1alpha) as markers of peri-implant tissue condition
.
Int J Oral Maxillofac Surg
.
2010
;
39
:
478
485
.
20
Liao
J,
Li
C,
Wang
Y,
et al.
Meta-analysis of the association between common interleukin-1 polymorphisms and dental implant failure
.
Mol Biol Rep
.
2014
;
41
:
2789
2798
.
21
Kornman
KS,
Crane
A,
Wang
HY,
et al.
The interleukin-1 genotype as a severity factor in adult periodontal disease
.
J Clin Periodontol
.
1997
;
24
:
72
77
.
22
Rogers
MA,
Figliomeni
L,
Baluchova
K,
et al.
Do interleukin-1 polymorphisms predict the development of periodontitis or the success of dental implants?
J Periodontal Res
.
2002
;
37
:
37
41
.
23
Greenstein
G,
Hart
TC.
A critical assessment of interleukin-1 (IL-1) genotyping when used in a genetic susceptibility test for severe chronic periodontitis
.
J Periodontol
.
2002
;
73
:
231
247
.
24
Hamdy
AA,
Ebrahem
MA.
The effect of interleukin-1 allele 2 genotype (IL-1a(-889) and IL-1b(+3954)) on the individual's susceptibility to peri-implantitis: case-control study
.
J Oral Implantol
.
2011
;
37
:
325
334
.
25
Hao
L,
Li
JL,
Yue
Y,
et al.
Application of interleukin-1 genes and proteins to monitor the status of chronic periodontitis
.
Int J Biol Markers
.
2013
;
28
:
92
99
.
26
Huynh-Ba
G,
Lang
NP,
Tonetti
MS,
Zwahlen
M,
Salvi
GE.
Association of the composite IL-1 genotype with peri-implantitis: a systematic review
.
Clin Oral Implants Res
.
2008
;
19
:
1154
1162
.
27
Andreiotelli
M,
Koutayas
SO,
Madianos
PN,
Strub
JR.
Relationship between interleukin-1 genotype and peri-implantitis: a literature review
.
Quintessence Int
.
2008
;
39
:
289
298
.
28
Lachmann
S,
Kimmerle-Muller
E,
Axmann
D,
Scheideler
L,
Weber
H,
Haas
R.
Associations between peri-implant crevicular fluid volume, concentrations of crevicular inflammatory mediators, and composite IL-1A-889 and IL-1B+3954 genotype: A cross-sectional study on implant recall patients with and without clinical signs of peri-implantitis
.
Clin Oral Implan Res
.
2007
;
18
:
212
223
.
29
Laine
ML,
Leonhardt
A,
Roos-Jansaker
AM,
et al.
IL-1RN gene polymorphism is associated with peri-implantitis
.
Clin Oral Implants Res
.
2006
;
17
:
380
385
.
30
Shimpuku
H,
Nosaka
Y,
Kawamura
T,
Tachi
Y,
Shinohara
M,
Ohura
K.
Genetic polymorphisms of the interleukin-1 gene and early marginal bone loss around endosseous dental implants
.
Clin Oral Implants Res
.
2003
;
14
:
423
429
.
31
Lin
YH,
Huang
P,
Lu
X,
et al.
The relationship between IL-1 gene polymorphism and marginal bone loss around dental implants
.
J Oral Maxillofac Surg
.
2007
;
65
:
2340
2344
.
32
Jaworska-Zaremba
M,
Mierzwinska-Nastalska
E,
Lomzynski
L,
Popko
K,
Wasik
M.
Analysis of genetic polymorphisms of the interleukin-1 gene in the implant prosthetic group of patients – preliminary studies
.
Cent Eur J Immunol
.
2008
;
33
:
74
77
.
33
Feloutzis
A,
Lang
NP,
Tonetti
MS,
et al.
IL-1 gene polymorphism and smoking as risk factors for peri-implant bone loss in a well-maintained population
.
Clin Oral Implants Res
.
2003
;
14
:
10
17
.
34
Wilson
TG
Jr,
Nunn
M.
The relationship between the interleukin-1 periodontal genotype and implant loss. Initial data
.
J Periodontol
.
1999
;
70
:
724
729
.
35
Campos
MI,
Santos
MC,
Trevilatto
PC,
Scarel-Caminaga
RM,
Bezerra
FJ,
Line
SR.
Evaluation of the relationship between interleukin-1 gene cluster polymorphisms and early implant failure in non-smoking patients
.
Clin Oral Implants Res
.
2005
;
16
:
194
201
.
36
Dirschnabel
AJ,
Alvim-Pereira
F,
Alvim-Pereira
CC,
Bernardino
JF,
Rosa
EA,
Trevilatto
PC.
Analysis of the association of IL1B(C-511T) polymorphism with dental implant loss and the clusterization phenomenon
.
Clin Oral Implants Res
.
2011
;
22
:
1235
1241
.
37
Gruica
B,
Wang
HY,
Lang
NP,
Buser
D.
Impact of IL-1 genotype and smoking status on the prognosis of osseointegrated implants
.
Clin Oral Implants Res
.
2004
;
15
:
393
400
.
38
Jansson
H,
Hamberg
K,
De Bruyn
H,
Bratthall
G.
Clinical consequences of IL-1 genotype on early implant failures in patients under periodontal maintenance
.
Clin Implant Dent Relat Res
.
2005
;
7
:
51
59
.
39
Montes
CC,
Alvim-Pereira
F,
de Castilhos
BB,
Sakurai
ML,
Olandoski
M,
Trevilatto
PC.
Analysis of the association of IL1B (C+3954T) and IL1RN (intron 2) polymorphisms with dental implant loss in a Brazilian population
.
Clin Oral Implants Res
.
2009
;
20
:
208
217
.
40
Vaz
P,
Gallas
MM,
Braga
AC,
Sampaio-Fernandes
JC,
Felino
A,
Tavares
P.
IL1 gene polymorphisms and unsuccessful dental implants
.
Clin Oral Implants Res
.
2012
;
23
:
1404
1413
.
41
Ries
WL,
Seeds
MC,
Key
LL.
Interleukin-2 stimulates osteoclastic activity: increased acid production and radioactive calcium release
.
J Periodontal Res
.
1989
;
24
:
242
246
.
42
Ishimi
Y,
Miyaura
C,
Jin
CH,
et al.
IL-6 is produced by osteoblasts and induces bone resorption
.
J Immunol
.
1990
;
145
:
3297
3303
.
43
Scarel-Caminaga
RM,
Trevilatto
PC,
Souza
AP,
Brito
RB,
Line
SR.
Investigation of an IL-2 polymorphism in patients with different levels of chronic periodontitis
.
J Clin Periodontol
.
2002
;
29
:
587
591
.
44
Trevilatto
PC,
Scarel-Caminaga
RM,
de Brito
RB,
de Souza
AP,
Line
SRP.
Polymorphism at position-174 of IL-6 gene is associated with susceptibility to chronic periodontitis in a Caucasian Brazilian population
.
J Clin Periodontol
.
2003
;
30
:
438
442
.
45
Franch-Chillida
F,
Nibali
L,
Madden
I,
Donos
N,
Brett
P.
Association between interleukin-6 polymorphisms and periodontitis in Indian non-smokers
.
J Clin Periodontol
.
2010
;
37
:
137
144
.
46
Nibali
L,
D'Aiuto
F,
Donos
N,
et al.
Association between periodontitis and common variants in the promoter of the interleukin-6 gene
.
Cytokine
.
2009
;
45
:
50
54
.
47
Nibali
L,
Griffiths
GS,
Donos
N,
et al.
Association between interleukin-6 promoter haplotypes and aggressive periodontitis
.
J Clin Periodontol
.
2008
;
35
:
193
198
.
48
Farhat
SB,
de Souza
CM,
Braosi
AP,
et al.
Complete physical mapping of IL6 reveals a new marker associated with chronic periodontitis
.
J Periodontal Res
.
2017
;
52
:
255
261
.
49
Campos
MI,
Godoy dos Santos MC, Trevilatto PC, Scarel-Caminaga RM, Bezerra FJ, Line SR. Interleukin-2 and interleukin-6 gene promoter polymorphisms, and early failure of dental implants
.
Implant Dent
.
2005
;
14
:
391
396
.
50
Reichow
AM,
Melo
AC,
de Souza
CM,
et al.
Outcome of orthodontic mini-implant loss in relation to interleukin 6 polymorphisms
.
Int J Oral Maxillofac Surg
.
2016
;
45
:
649
657
.
51
Scarel-Caminaga
RM,
Trevilatto
PC,
Souza
AP,
Brito
RB,
Jr.,
Line
SR.
Investigation of IL4 gene polymorphism in individuals with different levels of chronic periodontitis in a Brazilian population
.
J Clin Periodontol
.
2003
;
30
:
341
345
.
52
Pigossi
SC,
Alvim-Pereira
F,
Alvim-Pereira
CC,
Trevilatto
PC,
Scarel-Caminaga
RM.
Association of interleukin 4 gene polymorphisms with dental implant loss
.
Implant Dent
.
2014
;
23
:
723
731
.
53
Gurol
C,
Kazazoglu
E,
Dabakoglu
B,
Korachi
M.
A comparative study of the role of cytokine polymorphisms interleukin-10 and tumor necrosis factor alpha in susceptibility to implant failure and chronic periodontitis
.
Int J Oral Maxillofac Implants
.
2011
;
26
:
955
960
.
54
Ribeiro
R,
Melo
R,
Tortamano Neto P, Vajgel A, Souza PR, Cimoes R. Polymorphisms of Il-10 (-1082) and RANKL (-438) genes and the failure of dental implants
.
Int J Dent
.
2017
;
2017
:
3901368
.
55
Scarel-Caminaga
RM,
Trevilatto
PC,
Souza
AP,
Brito
RB,
Camargo
LE,
Line
SR.
Interleukin 10 gene promoter polymorphisms are associated with chronic periodontitis
.
J Clin Periodontol
.
2004
;
31
:
443
448
.
56
Schaefer
AS,
Bochenek
G,
Manke
T,
et al.
Validation of reported genetic risk factors for periodontitis in a large-scale replication study
.
J Clin Periodontol
.
2013
;
40
:
563
572
.
57
Kadkhodazadeh
M,
Baghani
Z,
Ebadian
AR,
Youssefi
N,
Mehdizadeh
AR,
Azimi
N.
IL-17 gene polymorphism is associated with chronic periodontitis and peri-implantitis in Iranian patients: a cross-sectional study
.
Immunol Invest
.
2013
;
42
:
156
163
.
58
Ohyama
H,
Kato-Kogoe
N,
Kuhara
A,
et al.
The involvement of IL-23 and the Th17 pathway in periodontitis
.
J Dent Res
.
2009
;
88
:
633
638
.
59
Takahashi
K,
Azuma
T,
Motohira
H,
Kinane
DF,
Kitetsu
S.
The potential role of interleukin-17 in the immunopathology of periodontal disease
.
J Clin Periodontol
.
2005
;
32
:
369
374
.
60
Bertolini
DR,
Nedwin
GE,
Bringman
TS,
Smith
DD,
Mundy
GR.
Stimulation of bone resorption and inhibition of bone formation in vitro by human tumour necrosis factors
.
Nature
.
1986
;
319
:
516
518
.
61
Johnson
RA,
Boyce
BF,
Mundy
GR,
Roodman
GD.
Tumors producing human tumor necrosis factor induced hypercalcemia and osteoclastic bone resorption in nude mice
.
Endocrinology
.
1989
;
124
:
1424
1427
.
62
Campos
MI,
dos Santos
MC,
Trevilatto
PC,
Scarel-Caminaga
RM,
Bezerra
FJ,
Line
SR.
Early failure of dental implants and TNF-alpha (G-308A) gene polymorphism
.
Implant Dent
.
2004
;
13
:
95
101
.
63
Cury
PR,
Joly
JC,
Freitas
N,
Sendyk
WR,
Nunes
FD,
de Araujo
NS.
Effect of tumor necrosis factor-alpha gene polymorphism on peri-implant bone loss following prosthetic reconstruction
.
Implant Dent
.
2007
;
16
:
80
88
.
64
Cury
PR,
Horewicz
VV,
Ferrari
DS,
et al.
Evaluation of the effect of tumor necrosis factor-alpha gene polymorphism on the risk of peri-implantitis: a case-control study
.
Int J Oral Maxillofac Implants
.
2009
;
24
:
1101
1105
.
65
Ding
C,
Ji
X,
Chen
X,
Xu
Y,
Zhong
L.
TNF-alpha gene promoter polymorphisms contribute to periodontitis susceptibility: evidence from 46 studies
.
J Clin Periodontol
.
2014
;
41
:
748
759
.
66
Song
GG,
Choi
SJ,
Ji
JD,
Lee
YH.
Association between tumor necrosis factor-alpha promoter -308 A/G, -238 A/G, interleukin-6 -174 G/C and -572 G/C polymorphisms and periodontal disease: a meta-analysis
.
Mol Biol Rep
.
2013
;
40
:
5191
5203
.
67
Rakic
M,
Petkovic-Curcin
A,
Struillou
X,
Matic
S,
Stamatovic
N,
Vojvodic
D.
CD14 and TNF-α single nucleotide polymorphisms are candidates for genetic biomarkers of peri-implantitis
.
Clin Oral Investig
.
2015
;
19
:
791
801
.
68
Mo
YY,
Zeng
XT,
Weng
H,
Cen
Y,
Zhao
Q,
Wen
X.
Association between tumor necrosis factor-alpha G-308A polymorphism and dental peri-implant disease risk: a meta-analysis
.
Medicine (Baltimore)
.
2016
;
95
:
e4425
.
69
Kadkhodazadeh
M,
Baghani
Z,
Ebadian
AR,
Kaghazchi
Z,
Amid
R.
Receptor activator of nuclear factor kappa-β gene polymorphisms in Iranian periodontitis and peri-implantitis patients
.
J Periodontal Implant Sci
.
2014
;
44
:
141
146
.
70
Kadkhodazadeh
M,
Ebadian
AR,
Gholami
GA,
Khosravi
A,
Tabari
ZA.
Analysis of RANKL gene polymorphism (rs9533156 and rs2277438) in Iranian patients with chronic periodontitis and periimplantitis
.
Arch Oral Biol
.
2013
;
58
:
530
536
.
71
Oum'hamed
Z,
Garnotel
R,
Josset
Y,
Trenteseaux
C,
Laurent-Maquin
D.
Matrix metalloproteinases MMP-2, -9 and tissue inhibitors TIMP-1, -2 expression and secretion by primary human osteoblast cells in response to titanium, zirconia, and alumina ceramics
.
J Biomed Mater Res A
.
2004
;
68
:
114
122
.
72
Takei
I,
Takagi
M,
Santavirta
S,
et al.
Messenger ribonucleic acid expression of 16 matrix metalloproteinases in bone-implant interface tissues of loose artificial hip joints
.
J Biomed Mater Res
.
2000
;
52
:
613
620
.
73
Thierbach
R,
Maier
K,
Sorsa
T,
Mantyla
P.
Peri-implant sulcus fluid (PISF) matrix metalloproteinase (MMP) -8 levels in peri-implantitis
.
J Clin Diagn Res.
2016
;
10:ZC34–38.
74
Ramseier
CA,
Eick
S,
Bronnimann
C,
Buser
D,
Bragger
U,
Salvi
GE.
Host-derived biomarkers at teeth and implants in partially edentulous patients. A 10-year retrospective study
.
Clin Oral Implants Res
.
2016
;
27
:
211
217
.
75
Leite
MF,
Santos
MC,
de Souza
AP,
Line
SR.
Osseointegrated implant failure associated with MMP-1 promotor polymorphisms (-1607 and -519)
.
Int J Oral Maxillofac Implants
.
2008
;
23
:
653
658
.
76
Santos
MC,
Campos
MI,
Souza
AP,
Trevilatto
PC,
Line
SR.
Analysis of MMP-1 and MMP-9 promoter polymorphisms in early osseointegrated implant failure
.
Int J Oral Maxillofac Implants
.
2004
;
19
:
38
43
.
77
Costa-Junior
FR,
Alvim-Pereira
CC,
Alvim-Pereira
F,
Trevilatto
PC,
de Souza
AP,
Santos
MC.
Influence of MMP-8 promoter polymorphism in early osseointegrated implant failure
.
Clin Oral Investig
.
2013
;
17
:
311
316
.
78
de Souza
AP,
Trevilatto
PC,
Scarel-Caminaga
RM,
Brito
RB,
Line
SR.
MMP-1 promoter polymorphism: association with chronic periodontitis severity in a Brazilian population
.
J Clin Periodontol
.
2003
;
30
:
154
158
.
79
Li
W,
Zhu
Y,
Singh
P,
Ajmera
DH,
Song
J,
Ji
P.
Association of Common Variants in MMPs with Periodontitis Risk
.
Dis Markers
.
2016
;
2016
:
1545974
.
80
de Souza
AP,
Trevilatto
PC,
Scarel-Caminaga
RM,
de Brito
RB
Jr,
Barros
SP,
Line
SR.
Analysis of the MMP-9 (C-1562 T) and TIMP-2 (G-418C) gene promoter polymorphisms in patients with chronic periodontitis
.
J Clin Periodontol
.
2005
;
32
:
207
211
.
81
Shimpuku
H,
Nosaka
Y,
Kawamura
T,
Tachi
Y,
Shinohara
M,
Ohura
K.
Bone morphogenetic protein-4 gene polymorphism and early marginal bone loss around endosseous implants
.
Int J Oral Maxillofac Implants
.
2003
;
18
:
500
504
.
82
Coelho
RB,
Goncalves
RJ,
Villas-Boas
Rde M,
et al.
Haplotypes in BMP4 and FGF genes increase the risk of peri-implantitis
.
Braz Dent J
.
2016
;
27
:
367
374
.
83
Connelly
JJ,
Shah
SH,
Doss
JF,
et al.
Genetic and functional association of FAM5C with myocardial infarction
.
BMC Med Genet
.
2008
;
9
:
33
.
84
Carvalho
FM,
Tinoco
EM,
Deeley
K,
et al.
FAM5C contributes to aggressive periodontitis
.
PLoS One
.
2010
;
5
:
e10053
.
85
Casado
PL,
Aguiar
DP,
Costa
LC,
et al.
Different contribution of BRINP3 gene in chronic periodontitis and peri-implantitis: a cross-sectional study
.
BMC Oral Health
.
2015
;
15
:
33
.
86
de Souza
AP,
Trevilatto
PC,
Scarel-Caminaga
RM,
de Brito
RB,
Line
SR.
Analysis of the TGF-beta1 promoter polymorphism (C-509T) in patients with chronic periodontitis
.
J Clin Periodontol
.
2003
;
30
:
519
523
.
87
Dos Santos
MC,
Campos
MI,
Souza
AP,
Scarel-Caminaga
RM,
Mazzonetto
R,
Line
SR.
Analysis of the transforming growth factor-beta 1 gene promoter polymorphisms in early osseointegrated implant failure
.
Implant Dent
.
2004
;
13
:
262
269
.
88
Richter
GM,
Graetz
C,
Pohler
P,
et al.
Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations
.
J Clin Periodontol
.
2012
;
39
:
315
322
.
89
Holla
LI,
Buckova
D,
Fassmann
A,
Roubalikova
L,
Vanek
J.
Lack of association between chronic periodontitis and the Toll-like receptor 4 gene polymorphisms in a Czech population
.
J Periodontal Res
.
2007
;
42
:
340
344
.
90
Nosaka
Y,
Tachi
Y,
Shimpuku
H,
Kawamura
T,
Ohura
K.
Association of calcitonin receptor gene polymorphism with early marginal bone loss around endosseous implants
.
Int J Oral Maxillofac Implants
.
2002
;
17
:
38
43
.
91
de Brito
RB,
Scarel-Caminaga
RMS,
Trevilatto
PC,
de Souza
AP,
Barros
SP.
Polymorphisms in the vitamin D receptor gene are associated with periodontal disease
.
J Periodontol
.
2004
;
75
:
1090
1095
.
92
Alvim-Pereira
F,
Montes
CC,
Thome
G,
Olandoski
M,
Trevilatto
PC.
Analysis of association of clinical aspects and vitamin D receptor gene polymorphism with dental implant loss
.
Clin Oral Implants Res
.
2008
;
19
:
786
795
.
93
Kadkhodazadeh
M,
Jafari
AR,
Amid
R,
et al.
MiR146a and MiR499 gene polymorphisms in Iranian periodontitis and peri-implantitis patients
.
J Long Term Eff Med Implants
.
2013
;
23
:
9
16
.
94
Shusterman
A,
Munz
M,
Richter
G,
et al.
The PF4/PPBP/CXCL5 gene cluster is associated with periodontitis
.
J Dent Res
.
2017
;
96
:
945
952
.
95
Munz
M,
Willenborg
C,
Richter
GM,
et al.
A genome-wide association study identifies nucleotide variants at SIGLEC5 and DEFA1A3 as risk loci for periodontitis
.
Hum Mol Genet
.
2017
;
26
:
2577
2588
.
96
Marchesan
JT,
Jiao
Y,
Moss
K,
et al.
Common polymorphisms in IFI16 and AIM2 genes are associated with periodontal disease
.
J Periodontol
.
2017
;
88
:
663
672
.
97
Shang
D,
Dong
L,
Zeng
L,
et al.
Two-stage comprehensive evaluation of genetic susceptibility of common variants in FBXO38, AP3B2 and WHAMM to severe chronic periodontitis
.
Sci Rep
.
2015
;
5
:
17882
.
98
Chen
G,
Zhou
D,
Zhang
Z,
et al.
Genetic variants in IFIH1 play opposite roles in the pathogenesis of psoriasis and chronic periodontitis
.
Int J Immunogenet
.
2012
;
39
:
137
143
.
99
Mengatto
CM,
Mussano
F,
Honda
Y,
Colwell
CS,
Nishimura
I.
Circadian rhythm and cartilage extracellular matrix genes in osseointegration: a genome-wide screening of implant failure by vitamin D deficiency
.
PLoS One
.
2011
;
6
:
e15848
.
100
Kadkhodazadeh
M,
Jafari
AR,
Khalighi
HR,
Ebadian
AR,
Vaziri
S,
Amid
R.
BRAF gene polymorphism (rs10487888) assessment in chronic periodontitis and peri-implantitis in an Iranian population
.
J Basic Clin Physiol Pharmacol
.
2013
;
24
:
131
135
.
101
Doetzer
AD,
Schlipf
N,
Alvim-Pereira
F,
et al.
Lactotransferrin gene (LTF) polymorphisms and dental implant loss: a case-control association study
.
Clin Implant Dent Relat Res
.
2015
;
17
(
suppl 2
):
e550
561
.
102
Ebadian
AR,
Kadkhodazadeh
M,
Naghavi
SH,
Torshabi
M,
Tamizi
M.
Haptoglobin gene polymorphisms in peri-implantitis and chronic periodontitis
.
J Investig Clin Dent
.
2014
;
5
:
125
130
.
103
Deas
DE,
Mikotowicz
JJ,
Mackey
SA,
Moritz
AJ.
Implant failure with spontaneous rapid exfoliation: case reports
.
Implant Dent
.
2002
;
11
:
235
242
.
104
Alvim-Pereira
F,
Montes
CC,
Mira
MT,
Trevilatto
PC.
Genetic susceptibility to dental implant failure: a critical review
.
Int J Oral Maxillofac Implants
.
2008
;
23
:
409
416
.
105
Hutton
JE,
Heath
MR,
Chai
JY,
et al.
Factors related to success and failure rates at 3-year follow-up in a multicenter study of overdentures supported by Branemark implants
.
Int J Oral Maxillofac Implants
.
1995
;
10
:
33
42
.
106
Dereka
X,
Mardas
N,
Chin
S,
Petrie
A,
Donos
N.
A systematic review on the association between genetic predisposition and dental implant biological complications
.
Clin Oral Implants Res
.
2012
;
23
:
775
788
.